The capacity of the NERVOUS SYSTEM to change its reactivity as the result of successive activations.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
A persistent increase in synaptic efficacy, usually induced by appropriate activation of the same synapses. The phenomenological properties of long-term potentiation suggest that it may be a cellular mechanism of learning and memory.
Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate via direct electrical coupling with ELECTRICAL SYNAPSES. Several other non-synaptic chemical or electric signal transmitting processes occur via extracellular mediated interactions.
A member of the nerve growth factor family of trophic factors. In the brain BDNF has a trophic action on retinal, cholinergic, and dopaminergic neurons, and in the peripheral nervous system it acts on both motor and sensory neurons. (From Kendrew, The Encyclopedia of Molecular Biology, 1994)
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.
A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity.
Relatively permanent change in behavior that is the result of past experience or practice. The concept includes the acquisition of knowledge.
Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory.
The observable response an animal makes to any situation.
A nervous tissue specific protein which is highly expressed in NEURONS during development and NERVE REGENERATION. It has been implicated in neurite outgrowth, long-term potentiation, SIGNAL TRANSDUCTION, and NEUROTRANSMITTER release. (From Neurotoxicology 1994;15(1):41-7) It is also a substrate of PROTEIN KINASE C.
The thin layer of GRAY MATTER on the surface of the CEREBRAL HEMISPHERES that develops from the TELENCEPHALON and folds into gyri and sulchi. It reaches its highest development in humans and is responsible for intellectual faculties and higher mental functions.
Spiny processes on DENDRITES, each of which receives excitatory input from one nerve ending (NERVE ENDINGS). They are commonly found on PURKINJE CELLS and PYRAMIDAL CELLS.
Extensions of the nerve cell body. They are short and branched and receive stimuli from other NEURONS.
Depolarization of membrane potentials at the SYNAPTIC MEMBRANES of target neurons during neurotransmission. Excitatory postsynaptic potentials can singly or in summation reach the trigger threshold for ACTION POTENTIALS.
Use of electric potential or currents to elicit biological responses.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Elements of limited time intervals, contributing to particular results or situations.
Almond-shaped group of basal nuclei anterior to the INFERIOR HORN OF THE LATERAL VENTRICLE of the TEMPORAL LOBE. The amygdala is part of the limbic system.
Formation of NEURONS which involves the differentiation and division of STEM CELLS in which one or both of the daughter cells become neurons.
A meshlike structure composed of interconnecting nerve cells that are separated at the synaptic junction or joined to one another by cytoplasmic processes. In invertebrates, for example, the nerve net allows nerve impulses to spread over a wide area of the net because synapses can pass information in any direction.
Refers to animals in the period of time just after birth.
In tissue culture, hairlike projections of neurons stimulated by growth factors and other molecules. These projections may go on to form a branched tree of dendrites or a single axon or they may be reabsorbed at a later stage of development. "Neurite" may refer to any filamentous or pointed outgrowth of an embryonal or tissue-culture neural cell.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
Neural tracts connecting one part of the nervous system with another.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Learning that takes place when a conditioned stimulus is paired with an unconditioned stimulus.
A class of ionotropic glutamate receptors characterized by their affinity for the agonist AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid).
GRAY MATTER situated above the GYRUS HIPPOCAMPI. It is composed of three layers. The molecular layer is continuous with the HIPPOCAMPUS in the hippocampal fissure. The granular layer consists of closely arranged spherical or oval neurons, called GRANULE CELLS, whose AXONS pass through the polymorphic layer ending on the DENDRITES of PYRAMIDAL CELLS in the hippocampus.
Peptides released by NEURONS as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells.
A protein that has been shown to function as a calcium-regulated transcription factor as well as a substrate for depolarization-activated CALCIUM-CALMODULIN-DEPENDENT PROTEIN KINASES. This protein functions to integrate both calcium and cAMP signals.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
A CELL LINE derived from a PHEOCHROMOCYTOMA of the rat ADRENAL MEDULLA. PC12 cells stop dividing and undergo terminal differentiation when treated with NERVE GROWTH FACTOR, making the line a useful model system for NERVE CELL differentiation.
Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Factors which enhance the growth potentialities of sensory and sympathetic nerve cells.
Learning the correct route through a maze to obtain reinforcement. It is used for human or animal populations. (Thesaurus of Psychological Index Terms, 6th ed)
Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.
A multifunctional calcium-calmodulin-dependent protein kinase subtype that occurs as an oligomeric protein comprised of twelve subunits. It differs from other enzyme subtypes in that it lacks a phosphorylatable activation domain that can respond to CALCIUM-CALMODULIN-DEPENDENT PROTEIN KINASE KINASE.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
The distal terminations of axons which are specialized for the release of neurotransmitters. Also included are varicosities along the course of axons which have similar specializations and also release transmitters. Presynaptic terminals in both the central and peripheral nervous systems are included.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
A protein-tyrosine kinase receptor that is specific for BRAIN-DERIVED NEUROTROPHIC FACTOR; NEUROTROPHIN 3; neurotrophin 4 and neurotrophin 5. It is widely expressed in nervous tissue and plays a role in mediating the effects of neurotrophins on growth and differentiation of neuronal cells.
The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
The function of opposing or restraining the excitation of neurons or their target excitable cells.
A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.
The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.
Projection neurons in the CEREBRAL CORTEX and the HIPPOCAMPUS. Pyramidal cells have a pyramid-shaped soma with the apex and an apical dendrite pointed toward the pial surface and other dendrites and an axon emerging from the base. The axons may have local collaterals but also project outside their cortical region.
Cellular DNA-binding proteins encoded by the c-fos genes (GENES, FOS). They are involved in growth-related transcriptional control. c-fos combines with c-jun (PROTO-ONCOGENE PROTEINS C-JUN) to form a c-fos/c-jun heterodimer (TRANSCRIPTION FACTOR AP-1) that binds to the TRE (TPA-responsive element) in promoters of certain genes.
The affective response to an actual current external danger which subsides with the elimination of the threatening condition.
A general term referring to the learning of some particular response.
A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.
An amino acid that, as the D-isomer, is the defining agonist for the NMDA receptor subtype of glutamate receptors (RECEPTORS, NMDA).
Area of the OCCIPITAL LOBE concerned with the processing of visual information relayed via VISUAL PATHWAYS.
An electrophysiologic technique for studying cells, cell membranes, and occasionally isolated organelles. All patch-clamp methods rely on a very high-resistance seal between a micropipette and a membrane; the seal is usually attained by gentle suction. The four most common variants include on-cell patch, inside-out patch, outside-out patch, and whole-cell clamp. Patch-clamp methods are commonly used to voltage clamp, that is control the voltage across the membrane and measure current flow, but current-clamp methods, in which the current is controlled and the voltage is measured, are also used.
Substances used for their pharmacological actions on any aspect of neurotransmitter systems. Neurotransmitter agents include agonists, antagonists, degradation inhibitors, uptake inhibitors, depleters, precursors, and modulators of receptor function.
The physical activity of a human or an animal as a behavioral phenomenon.
Cell-surface proteins that bind glutamate and trigger changes which influence the behavior of cells. Glutamate receptors include ionotropic receptors (AMPA, kainate, and N-methyl-D-aspartate receptors), which directly control ion channels, and metabotropic receptors which act through second messenger systems. Glutamate receptors are the most common mediators of fast excitatory synaptic transmission in the central nervous system. They have also been implicated in the mechanisms of memory and of many diseases.
An intermediate filament protein found only in glial cells or cells of glial origin. MW 51,000.
(2S-(2 alpha,3 beta,4 beta))-2-Carboxy-4-(1-methylethenyl)-3-pyrrolidineacetic acid. Ascaricide obtained from the red alga Digenea simplex. It is a potent excitatory amino acid agonist at some types of excitatory amino acid receptors and has been used to discriminate among receptor types. Like many excitatory amino acid agonists it can cause neurotoxicity and has been used experimentally for that purpose.
The absence or restriction of the usual external sensory stimuli to which the individual responds.
Protein analogs and derivatives of the Aequorea victoria green fluorescent protein that emit light (FLUORESCENCE) when excited with ULTRAVIOLET RAYS. They are used in REPORTER GENES in doing GENETIC TECHNIQUES. Numerous mutants have been made to emit other colors or be sensitive to pH.
Theoretical representations that simulate the behavior or activity of the neurological system, processes or phenomena; includes the use of mathematical equations, computers, and other electronic equipment.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or "seizure disorder."
A persistent activity-dependent decrease in synaptic efficacy between NEURONS. It typically occurs following repeated low-frequency afferent stimulation, but it can be induced by other methods. Long-term depression appears to play a role in MEMORY.
Signal transduction mechanisms whereby calcium mobilization (from outside the cell or from intracellular storage pools) to the cytoplasm is triggered by external stimuli. Calcium signals are often seen to propagate as waves, oscillations, spikes, sparks, or puffs. The calcium acts as an intracellular messenger by activating calcium-responsive proteins.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
The rostral part of the frontal lobe, bounded by the inferior precentral fissure in humans, which receives projection fibers from the MEDIODORSAL NUCLEUS OF THE THALAMUS. The prefrontal cortex receives afferent fibers from numerous structures of the DIENCEPHALON; MESENCEPHALON; and LIMBIC SYSTEM as well as cortical afferents of visual, auditory, and somatic origin.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
The functional superiority and preferential use of one eye over the other. The term is usually applied to superiority in sighting (VISUAL PERCEPTION) or motor task but not difference in VISUAL ACUITY or dysfunction of one of the eyes. Ocular dominance can be modified by visual input and NEUROTROPHIC FACTORS.
One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.
A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in ALCOHOLIC BEVERAGES.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in NERVE TISSUE.
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma.
An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
A specific stage in animal and human development during which certain types of behavior normally are shaped and molded for life.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
A group of severe neurodegenerative diseases characterized by intracellular accumulation of autofluorescent wax-like lipid materials (CEROID; LIPOFUSCIN) in neurons. There are several subtypes based on mutations of the various genes, time of disease onset, and severity of the neurological defects such as progressive DEMENTIA; SEIZURES; and visual failure.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Area of the parietal lobe concerned with receiving sensations such as movement, pain, pressure, position, temperature, touch, and vibration. It lies posterior to the central sulcus.
The non-genetic biological changes of an organism in response to challenges in its ENVIRONMENT.
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.
One of four subsections of the hippocampus described by Lorente de No, located furthest from the DENTATE GYRUS.
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
The largest portion of the CEREBRAL CORTEX in which the NEURONS are arranged in six layers in the mammalian brain: molecular, external granular, external pyramidal, internal granular, internal pyramidal and multiform layers.
An outbred strain of rats developed in 1915 by crossing several Wistar Institute white females with a wild gray male. Inbred strains have been derived from this original outbred strain, including Long-Evans cinnamon rats (RATS, INBRED LEC) and Otsuka-Long-Evans-Tokushima Fatty rats (RATS, INBRED OLETF), which are models for Wilson's disease and non-insulin dependent diabetes mellitus, respectively.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Most generally any NEURONS which are not motor or sensory. Interneurons may also refer to neurons whose AXONS remain within a particular brain region in contrast to projection neurons, which have axons projecting to other brain regions.
Stiff hairs projecting from the face around the nose of most mammals, acting as touch receptors.
A technique for maintenance or growth of animal organs in vitro. It refers to three-dimensional cultures of undisaggregated tissue retaining some or all of the histological features of the tissue in vivo. (Freshney, Culture of Animal Cells, 3d ed, p1)
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
The most common inhibitory neurotransmitter in the central nervous system.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action during the developmental stages of an organism.
Neurons which activate MUSCLE CELLS.
The anterior of the three primitive cerebral vesicles of the embryonic brain arising from the NEURAL TUBE. It subdivides to form DIENCEPHALON and TELENCEPHALON. (Stedmans Medical Dictionary, 27th ed)
The region of the cerebral cortex that receives the auditory radiation from the MEDIAL GENICULATE BODY.
Paired bodies containing mostly GRAY MATTER and forming part of the lateral wall of the THIRD VENTRICLE of the brain.
Area of the FRONTAL LOBE concerned with primary motor control located in the dorsal PRECENTRAL GYRUS immediately anterior to the central sulcus. It is comprised of three areas: the primary motor cortex located on the anterior paracentral lobule on the medial surface of the brain; the premotor cortex located anterior to the primary motor cortex; and the supplementary motor area located on the midline surface of the hemisphere anterior to the primary motor cortex.
The voltages across pre- or post-SYNAPTIC MEMBRANES.
Drugs that bind to and activate excitatory amino acid receptors.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.
A MARVEL domain-containing protein found in the presynaptic vesicles of NEURONS and NEUROENDOCRINE CELLS. It is commonly used as an immunocytochemical marker for neuroendocrine differentiation.
The entire nerve apparatus, composed of a central part, the brain and spinal cord, and a peripheral part, the cranial and spinal nerves, autonomic ganglia, and plexuses. (Stedman, 26th ed)
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
The output neurons of the cerebellar cortex.
Imaging techniques used to colocalize sites of brain functions or physiological activity with brain structures.
Cell surface proteins that bind glutamate and act through G-proteins to influence second messenger systems. Several types of metabotropic glutamate receptors have been cloned. They differ in pharmacology, distribution, and mechanisms of action.
Specialized afferent neurons capable of transducing sensory stimuli into NERVE IMPULSES to be transmitted to the CENTRAL NERVOUS SYSTEM. Sometimes sensory receptors for external stimuli are called exteroceptors; for internal stimuli are called interoceptors and proprioceptors.
The entity of a developing mammal (MAMMALS), generally from the cleavage of a ZYGOTE to the end of embryonic differentiation of basic structures. For the human embryo, this represents the first two months of intrauterine development preceding the stages of the FETUS.
Self-renewing cells that generate the main phenotypes of the nervous system in both the embryo and adult. Neural stem cells are precursors to both NEURONS and NEUROGLIA.
The number of CELLS of a specific kind, usually measured per unit volume or area of sample.
Set of cell bodies and nerve fibers conducting impulses from the eyes to the cerebral cortex. It includes the RETINA; OPTIC NERVE; optic tract; and geniculocalcarine tract.
Nerve structures through which impulses are conducted from a peripheral part toward a nerve center.
Investigative technique commonly used during ELECTROENCEPHALOGRAPHY in which a series of bright light flashes or visual patterns are used to elicit brain activity.
One of the two major classes of cholinergic receptors. Nicotinic receptors were originally distinguished by their preference for NICOTINE over MUSCARINE. They are generally divided into muscle-type and neuronal-type (previously ganglionic) based on pharmacology, and subunit composition of the receptors.
Use of sound to elicit a response in the nervous system.
Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures.
Drugs that bind to but do not activate GABA RECEPTORS, thereby blocking the actions of endogenous GAMMA-AMINOBUTYRIC ACID and GABA RECEPTOR AGONISTS.
The time from the onset of a stimulus until a response is observed.
NERVE GROWTH FACTOR is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Electrical responses recorded from nerve, muscle, SENSORY RECEPTOR, or area of the CENTRAL NERVOUS SYSTEM following stimulation. They range from less than a microvolt to several microvolts. The evoked potential can be auditory (EVOKED POTENTIALS, AUDITORY), somatosensory (EVOKED POTENTIALS, SOMATOSENSORY), visual (EVOKED POTENTIALS, VISUAL), or motor (EVOKED POTENTIALS, MOTOR), or other modalities that have been reported.
Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.
A family of synaptic vesicle-associated proteins involved in the short-term regulation of NEUROTRANSMITTER release. Synapsin I, the predominant member of this family, links SYNAPTIC VESICLES to ACTIN FILAMENTS in the presynaptic nerve terminal. These interactions are modulated by the reversible PHOSPHORYLATION of synapsin I through various signal transduction pathways. The protein is also a substrate for cAMP- and CALCIUM-CALMODULIN-DEPENDENT PROTEIN KINASES. It is believed that these functional properties are also shared by synapsin II.
A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes.
The D-enantiomer is a potent and specific antagonist of NMDA glutamate receptors (RECEPTORS, N-METHYL-D-ASPARTATE). The L form is inactive at NMDA receptors but may affect the AP4 (2-amino-4-phosphonobutyrate; APB) excitatory amino acid receptors.
An opisthobranch mollusk of the order Anaspidea. It is used frequently in studies of nervous system development because of its large identifiable neurons. Aplysiatoxin and its derivatives are not biosynthesized by Aplysia, but acquired by ingestion of Lyngbya (seaweed) species.
The external elements and conditions which surround, influence, and affect the life and development of an organism or population.
The electrical response evoked in a muscle or motor nerve by electrical or magnetic stimulation. Common methods of stimulation are by transcranial electrical and TRANSCRANIAL MAGNETIC STIMULATION. It is often used for monitoring during neurosurgery.
The electrical properties, characteristics of living organisms, and the processes of organisms or their parts that are involved in generating and responding to electrical charges.
ANIMALS whose GENOME has been altered by GENETIC ENGINEERING, or their offspring.
Peptides generated from AMYLOID BETA-PEPTIDES PRECURSOR. An amyloid fibrillar form of these peptides is the major component of amyloid plaques found in individuals with Alzheimer's disease and in aged individuals with trisomy 21 (DOWN SYNDROME). The peptide is found predominantly in the nervous system, but there have been reports of its presence in non-neural tissue.
Neurons whose primary neurotransmitter is GAMMA-AMINOBUTYRIC ACID.
Established cell cultures that have the potential to propagate indefinitely.
The part of the brain that connects the CEREBRAL HEMISPHERES with the SPINAL CORD. It consists of the MESENCEPHALON; PONS; and MEDULLA OBLONGATA.
A technique that involves the use of electrical coils on the head to generate a brief magnetic field which reaches the CEREBRAL CORTEX. It is coupled with ELECTROMYOGRAPHY response detection to assess cortical excitability by the threshold required to induce MOTOR EVOKED POTENTIALS. This method is also used for BRAIN MAPPING, to study NEUROPHYSIOLOGY, and as a substitute for ELECTROCONVULSIVE THERAPY for treating DEPRESSION. Induction of SEIZURES limits its clinical usage.
A light microscopic technique in which only a small spot is illuminated and observed at a time. An image is constructed through point-by-point scanning of the field in this manner. Light sources may be conventional or laser, and fluorescence or transmitted observations are possible.
The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Hyperpolarization of membrane potentials at the SYNAPTIC MEMBRANES of target neurons during NEUROTRANSMISSION. They are local changes which diminish responsiveness to excitatory signals.
The process of moving proteins from one cellular compartment (including extracellular) to another by various sorting and transport mechanisms such as gated transport, protein translocation, and vesicular transport.
Changes in the amounts of various chemicals (neurotransmitters, receptors, enzymes, and other metabolites) specific to the area of the central nervous system contained within the head. These are monitored over time, during sensory stimulation, or under different disease states.
High molecular weight proteins found in the MICROTUBULES of the cytoskeletal system. Under certain conditions they are required for TUBULIN assembly into the microtubules and stabilize the assembled microtubules.
Type III intermediate filament proteins that assemble into neurofilaments, the major cytoskeletal element in nerve axons and dendrites. They consist of three distinct polypeptides, the neurofilament triplet. Types I, II, and IV intermediate filament proteins form other cytoskeletal elements such as keratins and lamins. It appears that the metabolism of neurofilaments is disturbed in Alzheimer's disease, as indicated by the presence of neurofilament epitopes in the neurofibrillary tangles, as well as by the severe reduction of the expression of the gene for the light neurofilament subunit of the neurofilament triplet in brains of Alzheimer's patients. (Can J Neurol Sci 1990 Aug;17(3):302)
The superficial GRAY MATTER of the CEREBELLUM. It consists of two main layers, the stratum moleculare and the stratum granulosum.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Cell surface proteins which bind GAMMA-AMINOBUTYRIC ACID and contain an integral membrane chloride channel. Each receptor is assembled as a pentamer from a pool of at least 19 different possible subunits. The receptors belong to a superfamily that share a common CYSTEINE loop.
Act of eliciting a response from a person or organism through physical contact.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
The processes whereby the internal environment of an organism tends to remain balanced and stable.
A pathway of fibers that originates in the lateral part of the ENTORHINAL CORTEX, perforates the SUBICULUM of the HIPPOCAMPUS, and runs into the stratum moleculare of the hippocampus, where these fibers synapse with others that go to the DENTATE GYRUS where the pathway terminates. It is also known as the perforating fasciculus.
Wormlike or grublike stage, following the egg in the life cycle of insects, worms, and other metamorphosing animals.
Sensory ganglia located on the dorsal spinal roots within the vertebral column. The spinal ganglion cells are pseudounipolar. The single primary branch bifurcates sending a peripheral process to carry sensory information from the periphery and a central branch which relays that information to the spinal cord or brain.

Modulation of long-term synaptic depression in visual cortex by acetylcholine and norepinephrine. (1/7650)

In a slice preparation of rat visual cortex, we discovered that paired-pulse stimulation (PPS) elicits a form of homosynaptic long-term depression (LTD) in the superficial layers when carbachol (CCh) or norepinephrine (NE) is applied concurrently. PPS by itself, or CCh and NE in the absence of synaptic stimulation, produced no lasting change. The LTD induced by PPS in the presence of NE or CCh is of comparable magnitude with that obtained with prolonged low-frequency stimulation (LFS) but requires far fewer stimulation pulses (40 vs 900). The cholinergic facilitation of LTD was blocked by atropine and pirenzepine, suggesting involvement of M1 receptors. The noradrenergic facilitation of LTD was blocked by urapidil and was mimicked by methoxamine, suggesting involvement of alpha1 receptors. beta receptor agonists and antagonists were without effect. Induction of LTD by PPS was inhibited by NMDA receptor blockers (completely in the case of NE; partially in the case of CCh), suggesting that one action of the modulators is to control the gain of NMDA receptor-dependent homosynaptic LTD in visual cortex. We propose that this is a mechanism by which cholinergic and noradrenergic inputs to the neocortex modulate naturally occurring receptive field plasticity.  (+info)

Activity-dependent metaplasticity of inhibitory and excitatory synaptic transmission in the lamprey spinal cord locomotor network. (2/7650)

Paired intracellular recordings have been used to examine the activity-dependent plasticity and neuromodulator-induced metaplasticity of synaptic inputs from identified inhibitory and excitatory interneurons in the lamprey spinal cord. Trains of spikes at 5-20 Hz were used to mimic the frequency of spiking that occurs in network interneurons during NMDA or brainstem-evoked locomotor activity. Inputs from inhibitory and excitatory interneurons exhibited similar activity-dependent changes, with synaptic depression developing during the spike train. The level of depression reached was greater with lower stimulation frequencies. Significant activity-dependent depression of inputs from excitatory interneurons and inhibitory crossed caudal interneurons, which are central elements in the patterning of network activity, usually developed between the fifth and tenth spikes in the train. Because these interneurons typically fire bursts of up to five spikes during locomotor activity, this activity-dependent plasticity will presumably not contribute to the patterning of network activity. However, in the presence of the neuromodulators substance P and 5-HT, significant activity-dependent metaplasticity of these inputs developed over the first five spikes in the train. Substance P induced significant activity-dependent depression of inhibitory but potentiation of excitatory interneuron inputs, whereas 5-HT induced significant activity-dependent potentiation of both inhibitory and excitatory interneuron inputs. Because these metaplastic effects are consistent with the substance P and 5-HT-induced modulation of the network output, activity-dependent metaplasticity could be a potential mechanism underlying the coordination and modulation of rhythmic network activity.  (+info)

CRE-mediated gene transcription in neocortical neuronal plasticity during the developmental critical period. (3/7650)

Neuronal activity-dependent processes are believed to mediate the formation of synaptic connections during neocortical development, but the underlying intracellular mechanisms are not known. In the visual system, altering the pattern of visually driven neuronal activity by monocular deprivation induces cortical synaptic rearrangement during a postnatal developmental window, the critical period. Here, using transgenic mice carrying a CRE-lacZ reporter, we demonstrate that a calcium- and cAMP-regulated signaling pathway is activated following monocular deprivation. We find that monocular deprivation leads to an induction of CRE-mediated lacZ expression in the visual cortex preceding the onset of physiologic plasticity, and this induction is dramatically downregulated following the end of the critical period. These results suggest that CRE-dependent coordinate regulation of a network of genes may control physiologic plasticity during postnatal neocortical development.  (+info)

Impairment of neocortical long-term potentiation in mice deficient of endothelial nitric oxide synthase. (4/7650)

The role of the possible retrograde messenger nitric oxide (NO) in the induction of long-term potentiation (LTP) was studied in supragranular layers of somatosensory cortical slices obtained from adult mice. High-frequency stimulation produced a slowly rising, long-lasting (50 min) and significant (P < 0.001) increase in the extracellular synaptic response by 23%. The induction of LTP was independent from activation of N-methyl-D-aspartate (NMDA) receptors, but prevented by bath application of NG-nitro-L-arginine methyl ester (L-NAME), indicating that one or several of the different NO synthases (NOS) produced NO within the postsynaptic neuron. No LTP could be induced in knockout mice lacking the endothelial NOS (eNOS) isoform. These data suggest that eNOS is involved in an NMDA receptor-independent form of LTP in the rodent cerebral cortex.  (+info)

Selective induction of LTP and LTD by postsynaptic [Ca2+]i elevation. (5/7650)

Long-term potentiation (LTP) and long-term depression (LTD), two prominent forms of synaptic plasticity at glutamatergic afferents to CA1 hippocampal pyramidal cells, are both triggered by the elevation of postsynaptic intracellular calcium concentration ([Ca2+]i). To understand how one signaling molecule can be responsible for triggering two opposing forms of synaptic modulation, different postsynaptic [Ca2+]i elevation patterns were generated by a new caged calcium compound nitrophenyl-ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid in CA1 pyramidal cells. We found that specific patterns of [Ca2+]i elevation selectively activate LTP or LTD. In particular, only LTP was triggered by a brief increase of [Ca2+]i with relatively high magnitude, which mimics the [Ca2+]i rise during electrical stimulation typically used to induce LTP. In contrast, a prolonged modest rise of [Ca2+]i reliably induced LTD. An important implication of the results is that both the amplitude and the duration of an intracellular chemical signal can carry significant biological information.  (+info)

Selective pruning of more active afferents when cat visual cortex is pharmacologically inhibited. (6/7650)

Activity-dependent competition is thought to guide the normal development of specific patterns of neural connections. Such competition generally favors more active inputs, making them larger and stronger, while less active inputs become smaller and weaker. We pharmacologically inhibited the activity of visual cortical cells and measured the three-dimensional structure of inputs serving the two eyes when one eye was occluded. The more active inputs serving the open eye actually became smaller than the deprived inputs from the occluded eye, which were similar to those in normal animals. These findings demonstrate in vivo that it is not the amount of afferent activity but the correlation between cortical and afferent activity that regulates the growth or retraction of these inputs.  (+info)

Expression of the rat homologue of the Drosophila fat tumour suppressor gene. (7/7650)

We have sequenced and defined the expression during rat embryogenesis of the protocadherin fat, the murine homologue of a Drosophila tumour suppressor gene. As previously described for human fat, the sequence encodes a large protocadherin with 34 cadherin repeats, five epidermal growth factor (EGF)-like repeats containing a single laminin A-G domain and a putative transmembrane portion followed by a cytoplasmic sequence. This cytoplasmic sequence shows homology to the b-catenin binding regions of classical cadherin cytoplasmic tails and also ends with a PDZ domain-binding motif. In situ hybridization studies at E15 show that fat is predominately expressed in fetal epithelial cell layers and in the CNS, although expression is also seen in tongue musculature and condensing cartilage. Within the CNS, expression is seen in the germinal regions and in areas of developing cortex, and this neural expression pattern is also seen at later embryonic (E18) and postnatal stages. No labelling was seen in adult tissues except in the CNS, where the remnant of the germinal zones, as well as the dentate gyrus, continue to express fat.  (+info)

Synaptic plasticity: regulated translation in dendrites. (8/7650)

Synaptic activity can induce neurons to synthesize proteins important for cognition and brain development. Recent results suggest this activity-induced protein synthesis is partially mediated by regulated translation within neuronal dendrites.  (+info)

Spike-timing dependent plasticity is a learning mechanism used extensively within neural modelling. The learning rule has been shown to allow a neuron to find the onset of a spatio-temporal pattern repeated among its afferents. In this thesis, the first question addressed is what does this neuron learn? With a spiking neuron model and linear prediction, evidence is adduced that the neuron learns two components: (1) the level of average background activity and (2) specific spike times of a pattern. Taking advantage of these findings, a network is developed that can train recognisers for longer spatio-temporal input signals using spike-timing dependent plasticity. Using a number of neurons that are mutually connected by plastic synapses and subject to a global winner-takes-all mechanism, chains of neurons can form where each neuron is selective to a different segment of a repeating input pattern, and the neurons are feedforwardly connected in such a way that both the correct stimulus and the ...
Supervisors: Ole Paulsen, Tanja Fuchsberger. Spike timing-dependent plasticity (STDP) is a physiologically relevant form of Hebbian learning, in which near coincident pre- and postsynaptic firing induces synaptic plasticity: Long term potentiation (LTP) is induced when the presynaptic spike precedes postsynaptic firing, and long term depression (LTD) when postsynaptic firing precedes the presynaptic spike [1]. However, these plasticity rules are profoundly influenced by neuromodulators [2]. Reward, novelty or surprise are correlated with neuromodulatory signals, such as dopamine, acetylcholine or noradrenaline, which modulate memories and behavioural outcome. They regulate STDP through various mechanisms, as they can control the biophysical properties of dendrites, including the dynamics of spike backpropagation, and can influence the state of kinases and phosphatases implicated in synaptic plasticity (Seol et al., 2007). In our laboratory we recently demonstrated a retroactive effect of ...
Cortical neurons receive balanced excitatory and inhibitory synaptic currents. Such a balance could be established and maintained in an experience-dependent manner by synaptic plasticity at inhibitory synapses. We show that this mechanism provides an explanation for the sparse firing patterns observed in response to natural stimuli and fits well with a recently observed interaction of excitatory and inhibitory receptive field plasticity. ... Our results suggest an essential role of inhibitory plasticity in the formation and maintenance of functional cortical circuitry ...
Long-term potentiation (LTP) and long-term depression (LTD) are generally assumed to be cellular correlates for learning and memory. Different types of LTP induction protocols differing in severity of stimulation can be distinguished in CA1 of the hippocampus. To better understand signaling mechanisms and involvement of neuromodulators such as dopamine in synaptic plasticity, less severe and more physiological low frequency induction protocols should be used. In the study which is reviewed here, critical determinants of spike timing-dependent plasticity (STDP) at hippocampal CA3-CA1 synapses were investigated. We found that dopamine via D1 receptor signaling, but not adrenergic signaling activated by the -adrenergic agonist isoproterenol, is important for successful expression of STDP at CA3-CA1 synapses. The dopamine effect on STDP is paralleled by changes in spike firing properties, thereby changing intrinsic excitability of postsynaptic CA1 neurons, and gating STDP,. Whereas β-adrenergic
To determine if classical conditioning produces general or specific modification of responses to acoustic conditioned stimuli (CS), frequency receptive fields (RF) of neurons in guinea pig auditory cortex were determined before and up to 24 h after fear conditioning. Highly specific RF plasticity ch …
The mammalian sensory neocortex exhibits experience-dependent plasticity such that neurons modify their response properties according to changes in sensory experience. The synaptic plasticity mechanism of long-term potentiation requiring calcium-calmodulin-dependent kinase type II (CaMKII) could underlie experience-dependent plasticity. Plasticity in adult mice can be induced by changes in the patterns of tactile input to the barrel cortex. This response is strongly depressed in adult mice that lack the gene encoding α-CaMKII, although adolescent animals are unaffected. Thus, α-CaMKII is necessary either for the induction or for the expression of plasticity in adult mice.. ...
Structure-based virtual screening for selecting potential drug candidates is usually challenged by how numerous false positives in a molecule library are excluded when receptor plasticity is considered. In this study, based on the binding energy landscape theory, a hypothesis that a true inhibitor can bind to different conformations of the binding site favorably was put forth, and related strategies to defeat this challenge were devised; reducing false positives when receptor plasticity is considered. The receptor in the study is the influenza A nucleoprotein, whose oligomerization is a requirement for RNA binding. The structural flexibility of influenza A nucleoprotein was explored by molecular dynamics simulations. The resultant distinctive structures and the crystal structure were used as receptor models in docking exercises in which two binding sites, the tail-loop binding pocket and the RNA binding site, were targeted with the Otava PrimScreen1 diversity-molecule library using the GOLD software.
Synaptic plasticity directs development of the nervous system and is thought to underlie memory storage in adult animals. A great deal of our current understanding of the role of AMPA receptors in synaptic plasticity comes from studies on developing cortex and cell cultures. In the present study, we instead focus on plasticity in mature neurons in the neocortex of adult animals. We find that the glutamate receptor 1 (GluR1) subunit of the AMPA receptor is involved in experience-dependent plasticity in adult cortex in vivo and that it acts in addition to neuronal nitric oxide synthase (αNOS1), an enzyme that produces the rapid synaptic signaling molecule nitric oxide (NO). Potentiation of the spared whisker response, following single whisker experience, is ∼33% less in GluR1-null mutants than in wild types. We found that the remaining plasticity depended on αNOS1. Potentiation was reduced by ,42% in the single αNOS1-null mutants and completely abolished in GluR1/αNOS1 double-knock-out mice. ...
Background. Synaptic plasticity is thought to be the cellular correlate for the formation of memory traces in the brain. Recently, spike-timing dependent plasticity has gained increased interest as a plausible physiological mechanism for the activity-dependent modification of synaptic strength. It might be fundamental for circuit refinement, map plasticity and the explanation of higher brain functions. It is not clear if spike-timing dependent plasticity is a universal learning rule based on simple biophysical mechanisms. The molecular signalling pathways involved are quite diverse and apparently use-dependent. The fundamental question is what determines the molecular machinery at a synaptic contact that translates electrical activity into a change in synaptic strength.Specific Aims. (1) The influence of active dendritic properties, which can result in the generation of local dendritic spikes, on changes in synaptic strength will be studied. They will have an important impact on the local ...
The plasticity of inhibitory transmission is expected to play a key role in the modulation of neuronal excitability and network function. Over the last two decades, the investigation of the determinants of inhibitory synaptic plasticity has allowed distinguishing presynaptic and postsynaptic mechanisms. While there has been a remarkable progress in the characterization of presynaptically-expressed plasticity of inhibition, the postsynaptic mechanisms of inhibitory long-term synaptic plasticity only begin to be unraveled. At postsynaptic level, the expression of inhibitory synaptic plasticity involves the rearrangement of the postsynaptic molecular components of the GABAergic synapse, including GABAA receptors, scaffold proteins and structural molecules. This implies a dynamic modulation of receptor intracellular trafficking and receptor surface lateral diffusion, along with regulation of the availability and distribution of scaffold proteins. This Review will focus on the mechanisms of the multifaceted
Neuroplasticity studies examining children with hemiparesis (CH) have focused predominantly on unilateral interventions. CH also have bimanual coordination impairments with bimanual interventions showing benefits. We explored neuroplasticity following hand-Arm bimanual intensive therapy (HABIT) of 60 hours in twelve CH (6 females, mean age 11 ± 3.6 y). Serial behavioral evaluations and MR imaging including diffusion tensor (DTI) and functional (fMRI) imaging were performed before, immediately after, and at 6-week follow-up. Manual skills were assessed repeatedly with the Assisting Hand Assessment, Childrens Hand Experience Questionnaire, and Jebsen-Taylor Test of Hand Function. Beta values, indicating the level of activation, and lateralization index (LI), indicating the pattern of brain activation, were computed from fMRI. White matter integrity of major fibers was assessed using DTI. 11/12 children showed improvement after intervention in at least one measure, with 8/12 improving on two or ...
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TY - JOUR. T1 - Beta-amyloid (25-35) induced impairments of hippocampal synaptic plasticity are dependent on stimulation-protocol, genetic background, and aggregation state. AU - Gengler, Simon. AU - Gault, Victor. AU - Harriott, Peter. AU - Holscher, Christian. PY - 2007. Y1 - 2007. M3 - Article. VL - 179. SP - 621. EP - 632. JO - Experimental Brain Research. JF - Experimental Brain Research. SN - 0014-4819. ER - ...
Bacterial morphological plasticity refers to changes in the shape and size that bacterial cells undergo when they encounter stressful environments. Although bacteria have evolved complex molecular strategies to maintain their shape, many are able to alter their shape as a survival strategy in response to protist predators, antibiotics, the immune response, and other threats. Normally, bacteria have different shapes and sizes which include coccus, rod and helical/spiral (among others less common) and that allow for their classification. For instance, rod shapes may allow bacteria to attach more readily in environments with shear stress (e.g., in flowing water). Cocci may have access to small pores, creating more attachment sites per cell and hiding themselves from external shear forces. Spiral bacteria combine some of the characteristics cocci (small footprints) and of filaments (more surface area on which shear forces can act) and the ability to form an unbroken set of cells to build biofilms. ...
The ability to generate action potentials (spikes) in response to synaptic input determines whether a neuron participates in information processing. How a developing neuron becomes an active participant in a circuit or whether this process is activity dependent is not known, especially as spike-dependent plasticity mechanisms would not be available to non-spiking neurons. Here we use the optic tectum of awake Xenopus laevis tadpoles to determine how a neuron becomes able to generate sensory-driven spikes in vivo. At the onset of vision, many tectal neurons do not exhibit visual spiking behavior, despite being intrinsically excitable and receiving visuotopically organized synaptic inputs. However, a brief period of visual stimulation can drive these neurons to start generating stimulus-driven spikes. This conversion relies upon a selective increase in glutamatergic input and requires depolarizing GABAergic transmission and NMDA receptor activation. This permissive form of experience-dependent plasticity
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Our overarching interest is in the question of how experience and deprivation modify synaptic connections in the brain. Experience-dependent synaptic plasticity is the physical substrate of memory, sculpts connections during postnatal development to determine the capabilities and limitations of brain functions, is responsible for the reorganization of the brain after damage, and is vulnerable in numerous psychiatric and neurological diseases and contributes to their symptoms.. Historically, our major efforts to address this question have been focused on the visual cortex and hippocampus. The visual cortex is a site of robust experience-dependent synaptic plasticity, exemplified by the consequences of temporary monocular deprivation (MD) during childhood. MD sets in motion a stereotyped choreography of synaptic modification whereby the deprived-eye inputs to visual cortex rapidly lose strength and, with a delay, the open-eye inputs undergo a compensatory gain in strength. The behavioral ...
TY - JOUR. T1 - Neurotrophins and synaptic plasticity. AU - Usrey, A Kimberley. AU - Katz, Lawrence C.. AU - Lo, Donald C.. PY - 1999. Y1 - 1999. N2 - Despite considerable evidence that neuronal activity influences the organization and function of circuits in the developing and adult brain, the molecular signals that translate activity into structural and functional changes in connections remain largely obscure. This review discusses the evidence implicating neurotrophins as molecular mediators of synaptic and morphological plasticity. Neurotrophins are attractive candidates for these roles because they and their receptors are expressed in areas of the brain that undergo plasticity, activity can regulate their levels and -secretion, and they regulate both synaptic transmission and neuronal growth. Although numerous experiments show demonstrable effects of neurotrophins on synaptic plasticity, the rules and mechanisms by which they exert their effects remain intriguingly elusive.. AB - Despite ...
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AD patients show after iTBS an impairment of LTP-like cortical plasticity forming a paradoxical LTD in comparison to HS. LTD-like cortical plasticity is similar between AD and HS. LTP-like cortical plasticity is not associated with age, but AD patients presenting with more altered LTP-like cortical plasticity have more-severe cognitive decline at 18 months. SAI is impaired in AD and shows a strong association with the individual age of subjects rather than with disease age of onset.. ...
A major hallmark of brain diseases is neuroinflammation. We are interested in how immune mediators affect synaptic plasticity. Particularly, our work focuses on better understanding how these factors influence intracellular calcium stores, i.e. the spine apparatus organelle, and how these changes alter the ability of neurons to express associative and homeostatic synaptic plasticity. We study the role of coagulation factors in this context and test whether these changes can be modified by rTMS.. Ben Shimon M*, Lenz M*, Ikenberg B, Becker D, Shavit Stein E, Chapmann J, Tanne D, Pick CG, Blatt I, Neufeld M, Vlachos A*, Maggio N*° (2015) Thrombin regulation of synaptic transmission and plasticity: implications for health and disease. Front Cel Neurosci. 9: 151.. Becker D, Deller T, Vlachos A° (2015) Tumor necrosis factor (TNF)-receptor 1 and 2 mediate homeostatic synaptic plasticity of denervated mouse dentate granule cells. Sci Rep. 5: 12726.. Strehl A, Lenz M, Itsekson-Hayosh Z, Becker D, ...
The role of dopamine in plasticity at glutamatergic synapses in the striatum is central to our understanding of basal ganglia functions and dopamine-dependent reward mechanisms. Long-term potentiation (LTP) and long-term depression (LTD) at these synapses are thought to be dependent on D1 and D2 dopamine receptors, respectively. However, the mechanisms of LTP and LTD in the striatum are controversial. Using brain slices from transgenic mice, Shen et al. show that LTP and LTD can occur in both D1- and D2-expressing neurons but with different molecular mechanisms. Dopaminergic modulation of plasticity is receptor and cell-type specific. The findings suggest that the control of bidirectional plasticity is not exerted through a monolithic mechanism, as previously asserted, but by cell-type-specific mechanisms depending on the subtype of dopamine receptor expressed.. W. Shen, M. Flajolet, P. Greengard, D. J. Surmeier, Dichotomous dopaminergic control of striatal synaptic plasticity. Science 321, ...
The Haas Lab has developed specific visual stimulation protocols consisted of different periods of light ON and OFF stimuli to induce plasticity or metaplasticity in the optic tectum of awake Xenopus laevis tadpoles (Dunfield and Haas, 2009, 2010; Chen et al. 2012). Using these experience-driven neuronal plasticity induction stimuli and two-photon time-lapse imaging of mitochondrial movement and dendritic arbor growth, and calcium imaging of neuronal activity of individual neurons in the intact and awake developing brain, we are looking at mitochondria localization and size in LTD and LTP neurons. Other imaging and molecular techniques are also being used to underline the specific mitochondria proteins that regulate synaptic plasticity. ...
Synaptic Plasticity. Synaptic Plasticity. I. Synaptic Plasticity (Excitatory spine synapses) Changes in synaptic strength are important for formation of memory. Short Term Plasticity (paired-pulse facilitation, short-term potentiation, synaptic depression) Slideshow 6690266 by lev-levine
Challenges in the pain field include translation from animal models to identification of novel targets for drug development for humans and developing strategies that lead to improvements in patient care. Toward this goal, the symposium featured presentations that reviewed advances in the basic science and clinical arenas. Timothy Brennan, Ph.D., M.D. (Associate Professor of Anesthesia and Pharmacology, University of Iowa, Iowa City, Iowa), discussed the Peripheral and Central Plasticity in an Animal Model of Incisional Pain and Gary Strichartz, Ph.D. (Professor of Anesthesia, Pharmacology and Biophysics, Harvard Medical School, Brigham and Womens Hospital, Boston, Massachusetts), reviewed Pharmacological Studies on Preventing or Modulating the Plastic Changes in Experimental Models of Incisional Pain. Additional presentations on Clinical Evidence for Neural Plasticity in the Postoperative Period: Its Relevance and Modulation and Persistent Pain following Surgery: Neurobiological ...
The efficacy of synaptic transmission changes depending on the neuronal activity in the central nervous system. Such synaptic plasticity underlies experience-dependent refinement of information proces
The results described above emphasize the importance of ion channels at the AIS, and how their location, biophysical properties, and distribution can be modified by activity. However, how activity directly regulates these AIS properties, and whether the phenomenon of AIS plasticity occurs during normal brain function or only in response to large perturbations in neuronal activity or pathological conditions remains unclear. One strategy to begin to elucidate the mechanisms regulating AIS plasticity is to determine how the AIS is assembled during development and then maintained over an organisms lifetime.. How do ion channels become enriched at the AIS? As described above, the AIS is highly enriched in a variety of ion channels and each interacts with scaffolding proteins that link to the flexible actin/βIV spectrin-based submembranous cytoskeleton (Fig. 1D). Two scaffolding proteins have been identified at the AIS: ankG and PSD-93. PSD-93 binds to the KV1 channels found at the AIS, and ...
Learning is primarily mediated by activity-dependent modifications of synaptic strength within neuronal circuits. We discovered that place fields in hippocampal area CA1 are produced by a synaptic potentiation notably different from Hebbian plasticity. Place fields could be produced in vivo in a single trial by potentiation of input that arrived seconds before and after complex spiking. The potentiated synaptic input was not initially coincident with action potentials or depolarization. This rule, named behavioral time scale synaptic plasticity, abruptly modifies inputs that were neither causal nor close in time to postsynaptic activation. In slices, five pairings of subthreshold presynaptic activity and calcium (Ca(2+)) plateau potentials produced a large potentiation with an asymmetric seconds-long time course. This plasticity efficiently stores entire behavioral sequences within synaptic weights to produce predictive place cell activity.. ...
Spike timing-dependent plasticity (STDP) is a strong candidate for an N-methyl-D-aspartate (NMDA) receptor-dependent form of synaptic plasticity that could underlie the development of receptive field properties in sensory neocortices. Whilst inductio
This lecture 1/15 is part of the Computational Modeling of Neuronal Plasticity Course that aims to teach users how to build a mathematical model of a neuron, its inputs, and its neuronal plasticity mechanisms, by writing your own Python program. This lecture provides users with a brief video introduction to the concepts that serves as a companion to the lecture notes and solution figures.. Authors: Florence I. Kleberg and Prof. Jochen Triesch. ...
Arm-amputation involves two powerful drivers for brain plasticity-sensory deprivation and altered use. However, research has largely focused on sensory deprivation and maladaptive change. Here we show that adaptive patterns of limb usage after amputation drive cortical plasticity. We report that individuals with congenital or acquired limb-absence vary in whether they preferentially use their intact hand or residual arm in daily activities. Using fMRI, we show that the deprived sensorimotor cortex is employed by whichever limb individuals are over-using. Individuals from either group that rely more on their intact hands (and report less frequent residual arm usage) showed increased intact hand representation in the deprived cortex, and increased white matter fractional anisotropy underlying the deprived cortex, irrespective of the age at which deprivation occurred. Our results demonstrate how experience-driven plasticity in the human brain can transcend boundaries that have been thought to limit
Citation: Freire, R., Cheng, H. 2004. Experience-dependent changes in the hippocampus of domestic chicks: a model for spatial memory. European Journal of Neuroscience. 20(4):1065-1068. Interpretive Summary: In the modern broiler industry, chickens housed in large groups do not space themselves evenly but instead crowd in particular areas, which may affect chicken health and increase mortality. One contributing factor may be a deficit in spatial skills arising from the absence of essential environmental factors during routine rearing. The present study was to examine whether chick spatial skills can be improved by experimental training at an early age. Compared to control chicks, experience-induced changes in brain morphology reported here suggest that early experience leads to changes in the hippocampus that appear to be related to the development of spatial memory. Enhanced spatial memory in chickens may result in improving their well-being by increasing their distribution and their skills to ...
Transcription of synaptic plasticity-related genes in patients with somnipathy combined with type 2 diabetes, Yi Zhang, Rui Ma, Shaohong Zou, Gaiyu Tong, Gulibakeranmu Abula, Manna
The long-term goal of our research is to understand the neural circuit basis of learning and memory. In this project, we aim to understand how neural circuits p...
Neural Plasticity: (also known as brain plasticity and neural plasticity) can be defined as the ability of the central nervous system (CNS) to adapt in res
In D2 MSNs (fig. S1), repeated pairing of a synaptic stimulation with a postsynaptic spike 5 ms later resulted in LTP of the synaptic response (Fig. 1D). In contrast, preceding synaptic stimulation (-10 ms) with a short burst of postsynaptic spikes induced LTD (Fig. 1E). There were no lasting alterations in synaptic strength with unpaired presynaptic or postsynaptic activity (fig. S1).. Previous studies of striatal LTD induced by conventional plasticity protocols have underscored the importance of D2 receptors (7, 8, 16). In D2 MSNs, timing-dependent LTD was disrupted by antagonizing D2 receptors with sulpiride (control n = 5; sulpiride n = 5; P , 0.05, Mann-Whitney rank sum test), suggesting a similar involvement of D2 receptors (Fig. 1F). Moreover, LTD was disrupted by antagonizing CB1 endocannabinoid (fig. S2) or mGluR5 glutamate receptors (fig. S3). The combination of presynaptic activity and activation of terminal CB1 receptors leads to a lasting reduction in glutamate release probability ...
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A cell-specific regulation of redox state thus balances plasticity and stability of cortical networks. Mistimed developmental trajectories of brain plasticity may underlie, in part, the pathophysiology of mental illness. Such prolonged developmental plasticity may, in turn, offer a therapeutic oppor …
The molecular mechanisms controlling the delivery and subsequent stabilization of AMPARs during synaptic plasticity are still poorly understood. Recent findings have suggested PSD-95 as candidate molecule in these processes (El-Husseini et al., 2000; Schnell et al., 2002; Beique, 2003). However, particularly in the light of findings from PSD-95 mutant mice that exhibit enhanced LTP (Migaud et al., 1998), it remained controversial whether and how PSD-95 participates in synaptic plasticity. Here, we show that PSD-95 controls AMPAR delivery during synaptic strengthening by LTP in vitro and during experience-driven synaptic plasticity in vivo. We use three criteria to establish this: First, expression of wt PSD-95 mimics, and second wt PSD-95 occludes AMPAR delivery during synaptic strengthening; third, dominant negative forms of PSD-95 block the incorporation of AMPAR during plasticity.. Several findings indicate that expression of PSD-95 mimics key aspects of LTP and experience-driven synaptic ...
Network structure determines the flow of electrical activity in every neural network and determines its functional and computational properties. Electrical activation of the neuron goes along with an intracellular increase in calcium which induces morphological alterations of the neuron on a slower time scale. Morphological changes, such as changes in dendritic spine and axonal bouton numbers as well as elongation, retraction and branching of axons and dendrites have direct impact on network connectivity (structural plasticity) even in the adult brain: As a consequence of morphological changes, synapses may break, new synapses can form and axonal branches can be re-routed. Rewired network connectivity, in turn, gives rise to an altered activity dynamic and may hold as a source for long term memory formation. Experimental data further support the notion that structural plasticity is not necessarily Hebbian-like but may serve as a neuronal mechanism to maintain electrical activity at a certain ...
Background and Purpose-This study was designed to compare the effects of high-intensity interval training (HIT) and moderate-intensity continuous training (MOD) on functional recovery and cerebral plasticity during the first 2 weeks following cerebral ischemia. Methods-Rats were randomized as follows: Control (n=15), SHAM (n=9), MCAO (n=13), MCAO-D1 (n=7), MOD (n=13) and HIT (n=13). Incremental tests were performed at day 1 (D1) and 14 (D14) to identify the running speed associated with the lactate threshold (SLT) and the maximal speed (Smax). Functional tests were performed at D1, D7 and D14. Microglia form, cytokines, p75NTR, KCC2 and NKCC1 expression were made at D15. Results-HIT was more effective to improve the endurance performance than MOD and induced a fast recovery of the impaired forelimb grip force. The Iba-1 positive cells with amoeboid form and the pro- and anti-inflammatory cytokine expression were lower in HIT group, mainly in the ipsilesional hemisphere. A p75NTR overexpression ...
They say people don’t change, but author Sean Young’s upcoming book, “Stick With It,” examines the science behind doing just that—and making it stick. Over the past fifteen years, Young has worked with the brightest minds in science to identify the psychological processes that affect behavioral change, and according to his book, his methods have achieved a “300 percent increase in lasting change for both individuals and groups.” In other words, by making use of Young’s techniques, you are three times as likely to be able to make a change in your life and permanently stick with it. Why is this important? Just take a look at the way many people handle their health. Do they stick with their diets? Do they routinely take their needed medications? Do they exercise every week? How about finances? Or their relationship habits? Allowing these important areas of our lives to go unexamined and uncontrolled is the source of a vast amount of pain and loss, but by
Signalling pathways leading to post-synaptic plasticity have been examined in many types of experimental studies, but a unified picture on how multiple biochemical pathways collectively shape neocortical plasticity is missing. We built a biochemically detailed model of post-synaptic plasticity describing CaMKII, PKA, and PKC pathways and their contribution to synaptic potentiation or depression. We developed a statistical AMPA-receptor-tetramer model, which permits the estimation of the AMPA-receptor-mediated maximal synaptic conductance based on numbers of GluR1s and GluR2s predicted by the biochemical signalling model. We show that our model reproduces neuromodulator-gated spike-timing-dependent plasticity as observed in the visual cortex and can be fit to data from many cortical areas, uncovering the biochemical contributions of the pathways pinpointed by the underlying experimental studies. Our model explains the dependence of different forms of plasticity on the availability of different ...
When a cell has to endure lasting changes in its environment that require it to actively transport more molecules than normal through the cell membra...
The long-term goal of this project is to identify thalamocortical network mechanisms involved in consolidating experience-dependent plasticity in the visual sys...
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In the mammalian dentate gyrus (DG) neurogenesis continues throughout life. Accumulating evidence suggests a unique contribution of adult-generated neurons in DG synaptic plasticity and hippocampal-mediated learning and memory functions. However, the precise involvement of adult neurogenesis to disease-related cognitive deficits still remains unclear. Intellectual disabilities are the most striking clinical features of Down Syndrome (DS) and are characterized by learning deficits and memory impairment, particularly in hippocampus-related functions. Accordingly, the Ts65Dn mouse model of DS recapitulate many hippocampal cognitive deficits of the human syndrome, and also show decreased adult neurogenesis and impaired DG synaptic plasticity. To elucidate the contribution of faulty adult neurogenesis to DG synaptic plasticity deficits and memory impairment in DS we have treated adult Ts65Dn mice with lithium, a widely used mood stabilizer that also promotes neurogenesis. Results showed that chronic ...
Activity-dependent long-term changes in synaptic efficacy are thought to be important in learning, memory formation, neuronal development and pathological states of neuronal excitability in the CNS. For the past two decades, numerous studies have investigated long-term changes in synaptic efficacy at excitatory glutamatergic synapses. Although inhibitory synapses are essential for proper functioning of the neuronal network, attention has focused only recently on describing and characterizing plasticity at these types of synapse. Not surprisingly, different forms of plasticity at GABAergic, and the closely related glycinergic, synapses have been reported in several regions of the brain. Here we review these different forms of plasticity and focus on their possible roles in developing and adult neuronal networks.
Research Interests The future aint what it used to be - Yogi Berra It is precisely because the future is unpredictable that the mammalian brain has evolved the capacity to acquire new information through sensory experiences, store this information as memories, and rapidly retrieve this information to modify behavior. But how do novel sensory experiences embed themselves in the fabric of the brain to form memories? This question drives the research in my laboratory, which examines the cellular and synaptic mechanisms of experience-dependent plasticity in the neocortex. Specifically, I am interested in understanding i) where experience-dependent plasticity is initiated in the cortical circuitry; ii) how experience regulates the growth or retraction of synapses; iii) whether plasticity is restricted to only a subset of synaptic connections; iv) what distinguishes critical period plasticity from adult plasticity; v) how synaptic plasticity is altered in the aging and diseased brain. Techniques: To ...
Previous studies have reported primary auditory cortex plasticity following vagus nerve stimulation (VNS) paired with a sound. Does this phenomenon extend to other fields in the auditory pathway? In this podcast, Editor-in-Chief Bill Yates talks with Dr. Michael S. Borland and Dr. Crystal Engineer (both from the University of Texas at Dallas) about their recent study, which is the first to to document both cortical and subcortical plasticity following VNS-sound pairing. Listen to learn about auditory plasticity, potential therapies for auditory processing disorders, and more! Listen Now. August 14, 2019. ...
The molecular basis for the decline in experience-dependent neural plasticity over age remains poorly understood. In visual cortex, the robust plasticity induced in juvenile mice by brief monocular deprivation during the critical period is abrogated by genetic deletion of Arc, an activity-dependent regulator of excitatory synaptic modification. Here, we report that augmenting Arc expression in adult mice prolongs juvenile-like plasticity in visual cortex, as assessed by recordings of ocular dominance (OD) plasticity in vivo. A distinguishing characteristic of juvenile OD plasticity is the weakening of deprived-eye responses, believed to be accounted for by the mechanisms of homosynaptic long-term depression (LTD). Accordingly, we also found increased LTD in visual cortex of adult mice with augmented Arc expression and impaired LTD in visual cortex of juvenile mice that lack Arc or have been treated in vivo with a protein synthesis inhibitor. Further, we found that although activity-dependent ...
This new research might unite neurobiologists studying circadian rhythms with those studying developmental brain plasticity, Kobayashi notes. It could open inquiries into the role of circadian rhythm genes beyond the visual system, including brain regions that control cognition and social behaviors.. Specifically, the findings may have implications for disorders such as autism and schizophrenia. A number of genes associated with mental illness were expressed differently in the PV-cells of Clock-deficient versus control mice. The Hensch group and others have long proposed a link between neurodevelopmental disorders and timing defects in critical periods of brain plasticity. And finally, factors that influence circadian rhythms-sleep deprivation, seasonal changes limiting sunlight exposure, night shift work, etc.-have been linked to mood disorders.. By implicating circadian rhythm genes in the control of developmental brain plasticity, the new study may help bridge these ideas and suggests that ...
We used the rat visual cortex as a model system to examine the changes in protein synthesis during experience-induced synaptic plasticity. Dark-rearing rats from birth results in a relatively immature visual cortex that maintains the high de- gree of synaptic plasticity characteristic of the critical period (Kirkwood et al., 1995). Exposure of dark-reared rats to light results in a rapid, robust and coordinated burst of experience- driven synaptic plasticity that can be readily monitored at the biochemical and electrophysiological level (Quinlan et al., 1999). In previous work, we showed that visual experience evokes the polyadenylation of ␣-CaMKII mRNA in visual cortex and the elevation of ␣-CaMKII protein in synaptic fractions from this brain region. Moreover, this increase was a direct result of new synthesis because it was sensitive to the translation inhibitor cycloheximide (Wu et al., 1998). Here we show that the experience-induced increase of ␣-CaMKII pro- tein does not require new ...
The activity-regulated cytoskeletal protein Arc (also known as Arg3.1) is required for long-term memory formation and synaptic plasticity. Arc expression is robustly induced by activity, and Arc protein localizes to both active synapses and the nucleus. Whereas its synaptic function has been examined, it is not clear why or how Arc is localized to the nucleus. We found that murine Arc nuclear expression is regulated by synaptic activity in vivo and in vitro. We identified distinct regions of Arc that control its localization, including a nuclear localization signal, a nuclear retention domain and a nuclear export signal. Arc localization to the nucleus promotes an activity-induced increase in the expression of promyelocytic leukemia nuclear bodies, which decreases GluA1 (also called Gria1) transcription and synaptic strength. We further show that Arc nuclear localization regulates homeostatic plasticity. Thus, Arc mediates the homeostatic response to increased activity by translocating to the ...
While stroke-related deaths have decreased in recent years, stroke is still the leading cause of long-term disability in the United States. Adequate rehabilitation is dependant upon plasticity, a multidimensional and adaptive process underlying recovery of function in both the human and rodent brain. The complexity of processes underlying plasticity in the central nervous system is still largely unknown, but manipulating this spontaneous state of the healing brain is of the utmost importance as it will allow maximum therapeutic effect. Characterization of lesion-induced local and remote rewiring, initial behavioral deficit and their long-term relationships to behavioral outcome are required to fill some of the gaps in our understanding of brain repair mechanisms after stroke. The experiments outlined in this dissertation take advantage of hypothesized neuroplasticity foundations of learning and memory, as well as an established model of forelimb motor cortex injury in rats in order to examine ...
TY - JOUR. T1 - Adult cortical plasticity depends on an early postnatal critical period. AU - Greenhill, Stuart D.. AU - Juczewski, Konrad. AU - de Haan, Annelies M.. AU - Seaton, Gillian. AU - Fox, Kevin. AU - Hardingham, Neil R.. N1 - This is the authors version of the work. It is posted here by permission of the AAAS for personal use, not for redistribution. The definitive version was published in Science on Volume 349 Issue 6246 24 July 2015], DOI: 10.1126/science.aaa8481. PY - 2015/7/24. Y1 - 2015/7/24. N2 - Development of the cerebral cortex is influenced by sensory experience during distinct phases of postnatal development known as critical periods. Disruption of experience during a critical period produces neurons that lack specificity for particular stimulus features, such as location in the somatosensory system. Synaptic plasticity is the agent by which sensory experience affects cortical development. Here, we describe, in mice, a developmental critical period that affects plasticity ...
Postnatal sensory experience plays a significant role in the maturation and synaptic stabilization of sensory cortices, such as the primary auditory cortex (A1). Here, we examined the effects of patterned sound deprivation (by rearing in continuous white noise, WN) during early postnatal life on short- and long-term plasticity of adult male rats using an|i| in vivo|/i| preparation (urethane anesthesia). Relative to age-matched control animals reared under unaltered sound conditions, rats raised in WN (from postnatal day 5 to 50–60) showed greater levels of long-term potentiation (LTP) of field potentials in A1 induced by theta-burst stimulation (TBS) of the medial geniculate nucleus (MGN). In contrast, analyses of short-term plasticity using paired-pulse stimulation (interstimulus intervals of 25–1000 ms) did not reveal any significant effects of WN rearing. However, LTP induction resulted in a significant enhancement of paired-pulse depression (PPD) for both rearing conditions|i|.
article{ef532af8-d218-4166-9ec2-b39930c591ef, abstract = {,p,Following stroke, complete cellular death in the ischemic brain area may ensue, with remaining brain areas undergoing tissue remodelling to various degrees. Experience-dependent brain plasticity exerted through an enriched environment (EE) promotes remodelling after central nervous system injury, such as stroke. Post-stroke tissue reorganization is modulated by growth inhibitory molecules differentially expressed within the ischemic hemisphere, like chondroitin sulfate proteoglycans found in perineuronal nets (PNNs). PNNs in the neocortex predominantly enwrap parvalbumin-containing GABAergic (PV/GABA) neurons, important in sensori-information processing. Here, we investigate how extracellular matrix (ECM) proteases and their inhibitors may participate in the regulation of PNN integrity during stroke recovery. Rats were subjected to photothrombotic stroke in the motor cortex, and functional deficits were assessed at 7 days of recovery. ...
Resum: Although there is a decline in brain plasticity across lifespan, neurons in certain areas of the adult brain retain the ability to undergo synaptic, dendritic and spine remodeling in response to different stimuli. This neuronal structural plasticity seems to be the basis for many cognitive processes and it is crucial for adaptive responses to aversive experiences and recovery from brain damage and disease. Among the numerous candidate molecules that have been identified for mediating this neuronal remodeling, cell adhesion molecules and, specially, the neural cell adhesion molecule (NCAM), are of particular interest. The addition of polysialic acid (PSA) to the NCAM is critical for the structural changes that underlie plasticity; not only because it prevents both homotypic and heterotypic NCAM bindings (anti-adhesive properties) but also because it interacts with a large number of molecules and signaling pathways that regulate synaptic strength. In consonance with this fact, PSA-NCAM ...
TY - JOUR. T1 - Neuronal networks and synaptic plasticity in Parkinsons disease. T2 - beyond motor deficits. AU - Calabresi, Paolo. AU - Galletti, Francesca. AU - Saggese, Emanuele. AU - Ghiglieri, Veronica. AU - Picconi, Barbara. PY - 2007. Y1 - 2007. N2 - The excitatory corticostriatal pathway, which plays a critical role in the building up and storage of adaptive motor behaviours, can undergo long-lasting, activity-dependent changes in the efficacy of synaptic transmission, named long-term potentiation (LTP) and long- term depression (LTD). Both forms of plasticity are thought to underlie motor learning and depend upon the concomitant activation of glutamatergic corticostriatal and dopaminergic nigrostriatal pathways. Accordingly, corticostriatal LTP and LTD are altered in Parkinsons Disease (PD) models. The dopamine (DA)/acetylcholine(Ach) synaptic unbalance could be responsible of some of the cognitive deficits described in PD patients. The impairment of DA/ACh-dependent cellular learning ...
Abstract. It is now accepted that immune molecules are not only present within the brain during pathology but they exert physiological functions in the healthy brain as well. Increasing evidence points to a neuro-modulatory role of cytokines and chemokines (CHEMOtactic cytoKINES) in basal transmission and plasticity processes where signaling between peri-synaptic astrocytes, microglia and neurons plays an important role. Nevertheless, the exact mechanisms as to how cytokines, and in particular chemokines, participate in the molecular and cellular processes thought to subserve memory formation, plasticity processes and responsiveness to environmental stimuli remain to be clarified. Interestingly, in in vitro preparations, molecules like TNF-a, interleukin (IL)-1ß, IL-6, CX3CL1, CXCL12, CCL2 and CCL3 are implicated in synaptic formation and scaling, in modulation of glutamatergic transmission, in plasticity and neurogenesis, in particular in the hippocampus. The hippocampus is an extremely ...
The two fundamental forms of short-term plasticity, short-term depression and facilitation, coexist at most synapses, but little is known about their interaction. Here, we studied the interplay between short-term depression and facilitation at calyx of Held synapses. Stimulation at a low frequency of 10 or 20 Hz, which is in the range of the spontaneous activity of these auditory neurons in vivo, induced synaptic depression. Surprisingly, an instantaneous increase of the stimulation frequency to 100 or 200 Hz following the low-frequency train uncovered a robust facilitation of EPSCs relative to the predepressed amplitude level. This facilitation decayed rapidly (similar to 30 ms) and depended on presynaptic residual Ca2+, but it was not caused by Ca2+ current facilitation. To probe the release probability of the remaining readily releasable vesicles following the low-frequency train we made presynaptic Ca2+ uncaging experiments in the predepressed state of the synapse. We found that low-frequency
Author Summary Recent brain imaging and neurophysiological studies suggest that the striatum, the start of the basal ganglia circuit, plays a major role in value-based decision making and behavioral disorders such as drug addiction. The plasticity of synaptic input from the cerebral cortex to output neurons of the striatum, which are medium spiny neurons, depends on interactions between glutamate input from the cortex and dopaminergic input from the midbrain. It also links sensory and cognitive states in the cortex with reward-oriented action outputs. The mechanisms involved in molecular cascades that transmit glutamate and dopamine inputs to changes in postsynaptic glutamate receptors are very complex and it is difficult to intuitively understand the mechanism. Therefore, a biochemical network model was constructed, and computer simulations were performed. The model reproduced dopamine-dependent and calcium-dependent forms of long-term depression (LTD) and potentiation (LTP) of corticostriatal synapses
Does severe acute pain provoke lasting changes in attentional and emotional mechanisms of pain-related processing? A longitudinal ...
Eventbrite - Lison Mage | Author, Coach, Speaker, Facilitator presents Conquer Overthinking And Make Lasting Changes - Thursday, August 5, 2021 at Hong Kong Online, Hong kong, HKI. Find event and ticket information.
Tinnitus is a phantom auditory sensation that reduces quality of life for millions of people worldwide, and for which there is no medical cure. Most cases of tinnitus are associated with hearing loss caused by ageing or noise exposure. Exposure to loud recreational sound is common among the young, and this group are at increasing risk of developing tinnitus.
The world was originally introduced to the concept of synaptic plasticity over 60 years ago, when Dr. Donald Hebb first clearly defined a physiological mechanism for learning and memory in his seminal work The Organization of Behavior. It took another 20 years for Bliss and Lomo to scientifically validate Hebbs postulate, and show that neurons could alter their ability to communicate with one another in a persistent manner. Together, these works started off what has grown to become the field of synaptic plasticity. The years following the initial discovery were exciting times for learning and memory young researchers like myself, and each discovery over the next 20 years seemed to push us closer to elucidating the biological mechanisms responsible for memory formation. This seemed particularly true in the mid-1980s when the NMDA receptor was being heralded as the key to learning and memory processes. However, more recently it has become obvious that the activation of membrane receptors is ...
TY - JOUR. T1 - Chapter 27 Neural Plasticity After Nerve Injury and Regeneration. AU - Navarro, Xavier. PY - 2009/1/1. Y1 - 2009/1/1. N2 - Injuries to the peripheral nerves result in partial or total loss of motor, sensory, and autonomic functions in the denervated segments of the body due to the interruption of axons, degeneration of distal nerve fibers, and eventual death of axotomized neurons. Functional deficits caused by nerve injuries can be compensated by reinnervation of denervated targets by regenerating injured axons or by collateral branching of undamaged axons, and remodeling of nervous system circuitry related to the lost functions. Plasticity of central connections may compensate functionally for the lack of adequate target reinnervation; however, plasticity has limited effects on disturbed sensory localization or fine motor control after injuries, and may even result in maladaptive changes, such as neuropathic pain and hyperreflexia. After axotomy, neurons shift from a transmitter ...
His recommendations for healthy life (brisk walking, entertaining sporting activities, etc.) can be found in many books. This is supposed to be a book on neuroplasticity. Unfortunately, you hardly find real recommendations on how we can handle problems by using neuroplasticity tools. Title of the book and chapters do not reflect the real subject ...
The trajectory of the somatic membrane potential of a cortical neuron exactly reflects the computations performed on its afferent inputs. However, the spikes of such a neuron are a very low-dimensional and discrete projection of this continually evolving signal. We explored the possibility that the neurons efferent synapses perform the critical computational step of estimating the membrane potential trajectory from the spikes. We found that short-term changes in synaptic efficacy can be interpreted as implementing an optimal estimator of this trajectory. Short-term depression arose when presynaptic spiking was sufficiently intense as to reduce the uncertainty associated with the estimate; short-term facilitation reflected structural features of the statistics of the presynaptic neuron such as up and down states. Our analysis provides a unifying account of a powerful, but puzzling, form of plasticity.. ...
Coupling the control of expression stochasticity (noise) to the ability of expression change (plasticity) can alter gene function and influence adaptation. A number of factors, such as transcription re-initiation, strong chromatin regulation or genome neighboring organization, underlie this coupling. However, these factors do not necessarily combine in equivalent ways and strengths in all genes. Can we identify then alternative architectures that modulate in distinct ways the linkage of noise and plasticity? Here we first show that strong chromatin regulation, commonly viewed as a source of coupling, can lead to plasticity without noise. The nature of this regulation is relevant too, with plastic but noiseless genes being subjected to general activators whereas plastic and noisy genes experience more specific repression. Contrarily, in genes exhibiting poor transcriptional control, it is translational efficiency what separates noise from plasticity, a pattern related to transcript length. This
GABAergic (GABA = gamma-aminobutyric acid) neurons from different brain regions contain high levels of parvalbumin, both in their soma and in their neurites. Parvalbumin is a slow Ca(2+) buffer that may affect the amplitude and time course of intracellular Ca(2+) transients in terminals after an action potential, and hence may regulate short-term synaptic plasticity. To test this possibility, we have applied paired-pulse stimulations (with 30- to 300-ms intervals) at GABAergic synapses between interneurons and Purkinje cells, both in wild-type (PV+/+) mice and in parvalbumin knockout (PV-/-) mice. We observed paired-pulse depression in PV+/+ mice, but paired-pulse facilitation in PV-/- mice. In paired recordings of connected interneuron-Purkinje cells, dialysis of the presynaptic interneuron with the slow Ca(2+) buffer EGTA (1 mM) rescues paired-pulse depression in PV-/- mice. These data show that parvalbumin potently modulates short-term synaptic plasticity. ...
This laboratory pilot study will explore the effects of varenicline tartrate on long-term potentiation (LTP)-like mechanisms of (1) the motor cortex and (2) the dorsolateral prefrontal cortex (DLPFC) and working memory in non-smoking patients with schizophrenia and healthy controls using a Paired Associative Stimulation (PAS) method. The present study will use this novel PAS method to evaluate the effects of five doses of varenicline (Champix) 0.5 mg BID treatment on neuroplasticity changes and working memory in 28 non-smokers with schizophrenia and 28 non-smoking controls in a placebo-controlled, double-blinded, cross-over design. The hypothesis is that varenicline will increase LTP-like facilitation of the DLPFC as compared with placebo in patients with schizophrenia, with less or a null effect in healthy controls. Likewise, it is hypothesized that varenicline will specifically improve working memory in patients with schizophrenia as compared with placebo and healthy controls. We Hypothesize ...
Valentina received her Ph.D. in Neuroscience from Tor Vergata University (Rome), where she explored the role of FMRP in the regulation of transport, translation and stability of dendritic mRNAs. Later she worked extensively on learning-dependent synaptic plasticity at the Hospital for Sick Children, Toronto.. Valentina ...
TY - CHAP. T1 - Translating memories. T2 - The role of protein biosynthesis in synpatic plasticity. AU - Westmark, Cara J.. AU - Malter, James S.. PY - 2009/1/1. Y1 - 2009/1/1. N2 - The 1990s, The Decade of the Brain, resulted in major scientific advances involving brain imaging, gene therapy, brain/robotic interfacing and the neurobiology and molecular biology of learning and memory. However, despite these critical insights, we still do not know exactly how thoughts or memories are formed or stored in the brain, which leaves much exciting research for the twenty-first and probably centuries to come. This review will elaborate on recent advances in the field of protein biosynthesis as related to synaptic plasticity. We will discuss the molecular players (RNA binding proteins and neuronal mRNAs), the signal transduction pathways that have been implicated in learning and memory and how localized translation of selected mRNAs is involved in synaptic plasticity. We will also discuss the pathology ...
Dopamine-dependent long-term depression at subthalamo-nigral synapses is lost in experimental parkinsonism.: Impairments of synaptic plasticity are a hallmark o
It is an open question how the multiple special and temporal scales involved in intracellular Ca2+ handling within the STDP models affect the plasticity outcomes predicted by these models. Hebbian or associative plasticity is triggered by postsynaptic Ca2+ influx which activates calmodulin and CaMKII. The influx of Ca2+ through voltage-dependent NMDA receptors and Ca2+ channels is regulated by Ca2+ -activated K+ channels (SK-channels) providing negative feedback regulation of postsynaptic [Ca2+]. Using 3-dimensional modelling of Ca2+ and calmodulin dynamics within dendritic spines we show that the non-linear relationship between Ca2+ influx and calmodulin activation endows SK-channels with the ability to gate calmodulin activation and therefore the induction of Hebbian synaptic plasticity. Since SK-channels are inhibited by several neuro-modulator receptors including acetylcholine and noradrenaline, the gating of synaptic plasticity by SK-channels could represent a common mechanism by which ...
We unravel how functional plasticity and redundancy are essential mechanisms underlying the ability to survive of metabolic networks. We perform an exhaustive computational screening of synthetic lethal reaction pairs in Escherichia coli in a minimal medium and we find that synthetic lethal pairs divide in two different groups depending on whether the synthetic lethal interaction works as a backup or as a parallel use mechanism, the first corresponding to essential plasticity and the second to essential redundancy. In E. coli, the analysis of pathways entanglement through essential redundancy supports the view that synthetic lethality affects preferentially a single function or pathway. In contrast, essential plasticity, the dominant class, tends to be inter-pathway but strongly localized and unveils Cell Envelope Biosynthesis as an essential backup for Membrane Lipid Metabolism. When comparing E. coli and Mycoplasma pneumoniae, we find that the metabolic networks of the two organisms exhibit a ...
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Maheu ME, Ressler KJ. Developmental pathway genes and neural plasticity underlying emotional learning and stress-related disorders. Learn Mem. 2017 09; 24(9):492-501 ...
If you have a question about this talk, please contact Dr Etienne Gaudrain.. Abstract not available. This talk is part of the Hearing Group Meetings series.. ...
Nitrogen (N) is central for plant growth, and metabolic plasticity can provide a strategy to respond to changing N availability. We showed that two local A. thaliana populations exhibited differential plasticity in the compounds of photorespiratory and starch degradation pathways in response to three N conditions. Association of metabolite levels with growth-related and fitness traits indicated that controlled plasticity in these pathways could contribute to local adaptation and play a role in plant evolution.
"Neuronal Plasticity Prize" (PDF). 2018. Retrieved 4 January 2021. "Feldberg Foundation for anglo-german scientific exchange - ... 1995 founder member of the Academia Europaea 1997 Neuronal Plasticity Prize (with Antonio Damasio and Michael Merzenich) 1997 ... These techniques made it possible to demonstrate the existence of the brain's dynamic neuronal plasticity, both in its ...
Neuronal specificity, plasticity, and patterns. Moscona, A. A. (Aron Arthur), 1922-2009,, Monroy, Alberto,, Hunt, R. Kevin. New ... The MAPs make-up of neurotubules is notably different from microtubules of non-neuronal cells. For example, type II MAPs are ... This action propels the soma of the neuron forward, which is an essential step in neuronal migration. In addition, mutations in ... LIS1 encodes an adaptor protein Lis1 that is responsible for stabilization of neurotubule during neuronal migration by ...
IPSEN Prize in Neuronal Plasticity, 1990[6]. *Charles A. Dana Award for Pioneering Achievements in Health and Education, 1993 ... and has concentrated on the adult central nervous system and the unexpected plasticity and adaptability that remains throughout ...
Single Neurons, Populations, Plasticity. Cambridge University Press. Latham, P. E., B. J. Richmond, P. G. Nelson, and S. ... 2000). "Intrinsic Dynamics in Neuronal Networks. I. Theory". Journal of Neurophysiology. 88 (2): 808-27. doi:10.1152/jn.2000.83 ... 2000). "Intrinsic Dynamics in Neuronal Networks. I. Theory". Journal of Neurophysiology. 88 (2): 808-27. doi:10.1152/jn.2000.83 ... 2000). "Intrinsic Dynamics in Neuronal Networks. I. Theory". Journal of Neurophysiology. 88 (2): 808-27. doi:10.1152/jn.2000.83 ...
Debanne, Dominique; Inglebert, Yanis; Russier, Michaël (2019). "Plasticity of intrinsic neuronal excitability" (PDF). Current ... In neuronal cells, an action potential begins with a rush of sodium ions into the cell through sodium channels, resulting in ... Goldin AL (2007). "Neuronal Channels and Receptors". In Waxman SG (ed.). Molecular Neurology. Burlington, MA: Elsevier Academic ... Activation of synaptic receptors initiates long-lasting changes in neuronal excitability. Thyroid, adrenal and other hormones ...
Turrigiano, G. G. (1999). "Homeostatic plasticity in neuronal networks: The more things change, the more they stay the same". ... Hebbian plasticity and homeostatic plasticity have a hand-in-glove relationship. Neurons use Hebbian plasticity mechanisms to ... Turrigiano, G. G.; Nelson, S. B. (2000). "Hebb and homeostasis in neuronal plasticity". Current Opinion in Neurobiology. 10 (3 ... Since homeostatic plasticity normalizes the synaptic strengths of all neurons in a network, the overall neural network activity ...
Eccles JC, Ito M, Szentágothai J (1967). The Cerebellum as a Neuronal Machine. Springer-Verlag. The Cerebellum as a Neuronal ... Plasticity: The synapses between parallel fibers and Purkinje cells, and the synapses between mossy fibers and deep nuclear ... Each part of the cortex consists of the same small set of neuronal elements, laid out in a highly stereotyped geometry. At an ... ISBN 978-0-03-910284-5. Shi Z, Zhang Y, Meek J, Qiao J, Han VZ (August 2008). "The neuronal organization of a unique cerebellar ...
... computational studies of neuronal oscillations and synchronization; neural plasticity; nonlinear dynamical systems theory and ... interests are cognitive neuroscience of attention and consciousness with special emphasis on EEG and MEG studies of neuronal ...
GAP43 is called a "growth" or "plasticity" protein because it is expressed at high levels in neuronal growth cones during ... Molecular and Cellular Mechanisms of Neuronal Plasticity. Advances in Experimental Medicine and Biology. 446. pp. 85-106. doi: ... an intrinsic determinant of neuronal development and plasticity". Trends in Neurosciences. 20 (2): 84-91. doi:10.1016/S0166- ... "Neuronal pathfinding is abnormal in mice lacking the neuronal growth cone protein GAP-43". Cell. 80 (3): 445-52. doi:10.1016/ ...
Gogolla co-first authored a paper in Neuron describing axonal plasticity mechanisms and the role of axonal plasticity in ... Neuronal and glial cell biology / New technologies. 17 (5): 516-524. doi:10.1016/j.conb.2007.09.002. ISSN 0959-4388. PMID ... Under the mentorship of Pico Caroni, Gogolla explored the regulatory mechanisms governing structural plasticity in the brain. ... Gogolla, Nadine; Galimberti, Ivan; Depaola, Vincenzo; Caroni, Pico (2006). "Long-term live imaging of neuronal circuits in ...
Since beta amyloid is a strong stimulant to CSPG production and CSPGs are inhibitory to neuronal growth and synaptic plasticity ... "Aggrecan Directs Extracellular Matrix-Mediated Neuronal Plasticity". Journal of Neuroscience. 38 (47): 10102-10113. doi:10.1523 ... Plasticity of intact areas in the brain stem and spinal cord also increases following spinal cord injury. The critical period ... Moreover, Golgi brought interest to the subject due to his opinion that the PNN was not a neuronal structure but rather a "kind ...
... and brain plasticity in clownfish. Rhodes research interests relate to neuronal plasticity. One interest includes understanding ... Currently, Rhodes has also established a marine biology laboratory to research brain plasticity in clownfish undergoing sex ...
"Glutamate and neurotrophic factors in neuronal plasticity and disease". Annals of the New York Academy of Sciences. 1144 (1): ... Arancio O, Chao MV (June 2007). "Neurotrophins, synaptic plasticity and dementia". Current Opinion in Neurobiology. 17 (3): 325 ... Penzes P, Johnson RC, Sattler R, Zhang X, Huganir RL, Kambampati V, Mains RE, Eipper BA (January 2001). "The neuronal Rho-GEF ... Briones TL, Suh E, Jozsa L, Hattar H, Chai J, Wadowska M (February 2004). "Behaviorally-induced ultrastructural plasticity in ...
"Glutamate and neurotrophic factors in neuronal plasticity and disease". Annals of the New York Academy of Sciences. 1144: 97- ... January 2008). "BHLHB2 controls Bdnf promoter 4 activity and neuronal excitability". The Journal of Neuroscience. 28 (5): 1118- ... Arancio O, Chao MV (June 2007). "Neurotrophins, synaptic plasticity and dementia". Current Opinion in Neurobiology. 17 (3): 325 ... Penzes P, Johnson RC, Sattler R, Zhang X, Huganir RL, Kambampati V, Mains RE, Eipper BA (January 2001). "The neuronal Rho-GEF ...
Benarroch EE (March 2007). "Neurosteroids: endogenous modulators of neuronal excitability and plasticity". Neurology. 68 (12): ... In addition to their actions on neuronal membrane receptors, some of these steroids may also exert effects on gene expression ... Melcangi RC, Celotti F, Martini L (March 1994). "Progesterone 5-alpha-reduction in neuronal and in different types of glial ... Some major known biological functions of neurosteroids include modulation of neural plasticity, learning and memory processes, ...
Lledo, Pierre-Marie; Alonso, Mariana; Grubb, Matthew S. (March 2006). "Adult neurogenesis and functional plasticity in neuronal ... Neuritic plaques, that target the outer regions of the cortex, consist of withering neuronal material from a protein, amyloid- ... Many of the contributing factors that may cause sarcopenia to include neuronal and hormonal changes, inadequate nutrition, and ... Mühlig-Versen, Andrea; Bowen, Catherine E.; Staudinger, Ursula M. (2012). "Personality plasticity in later adulthood: ...
This also increases the potential for neuronal plasticity. Generally, these antidepressants increase peripheral BDNF levels by ... Karpova NN (January 2014). "Role of BDNF epigenetics in activity-dependent neuronal plasticity". Neuropharmacology. 76 Pt C: ... which is involved in neuronal plasticity. In rats, it has been shown that individuals less susceptible to depressive behavior ... Because MeCP2 can no longer bind to the BDNF promoter and repress transcription, BDNF levels increase and neuronal development ...
Berlucchi, G.; Buchtel, H. A. (1 January 2009). "Neuronal plasticity: historical roots and evolution of meaning". Experimental ... and Ernesto Lugaro was later responsible for the association of neural plasticity with synaptic plasticity. It wasn't until ... "Plasticity" was made popular by Livingstons work in 1966. He challenged the consensus that the brain only develops during a ... This led him to believe that neural plasticity was possible, and the brain of an adult rhesus monkey was able to incorporate ...
NgR is implicated in neuronal plasticity and regeneration. Its relative importance in mediating myelin inhibition in vitro and ... such that adult plasticity in the mutant mice resembled normal visual plasticity in juvenile mice brains. This function of NgR ... McGee, A. W.; Yang, Y; Fischer, Q. S.; Daw, N. W.; Strittmatter, S. M. (2005). "Experience-driven plasticity of visual cortex ... While the entire pathway is not fully understood, the relationship between NgR and neuronal outgrowth has been fleshed out. NgR ...
Bading, H. (2000-09-01). "Transcription-dependent neuronal plasticity: the nuclear calcium hypothesis". European Journal of ...
Neuronal plasticity, or the capability of the brain to adapt to new requirements, is a prime example of plasticity stressing ... Röder, B. (2006). Blindness: A source and case of neuronal plasticity. In P. Baltes, P. Reuter-Lorenz, & F. Rösler (Eds.), ... Plasticity is imperative to current research because the potential for intervention is derived from the notion of plasticity in ... In the end, neuronal changes to the limbic system and prefrontal cortex which are associated with puberty lead to the ...
GAP43 has been termed a 'growth' or 'plasticity' protein because it is expressed at high levels in neuronal growth cones during ... Benowitz LI, Routtenberg A (Feb 1997). "GAP-43: an intrinsic determinant of neuronal development and plasticity". Trends in ... "Neuronal pathfinding is abnormal in mice lacking the neuronal growth cone protein GAP-43". Cell. 80 (3): 445-52. doi:10.1016/ ... Pp46 was concentrated in neuronal growth cones and was thus postulated to play an important role in brain development. In the ...
Several studies suggest it has a role in neuronal plasticity.[5] EGR-1 is an important transcription factor in memory formation ... Knapska E, Kaczmarek L (2004). "A gene for Neuronal Plasticity in the Mammalian Brain: Zif286/Egr1/NGFI-A/Krox-24/TIS-8/ZENK ... in learning and in long-term neuronal plasticity. EGR-1 has also been found to regulate the expression of VAMP2 (a protein ... It has a distinct pattern of expression in the brain, and its induction has been shown to be associated with neuronal activity ...
Kaech S, Ludin B, Matus A (1996). "Cytoskeletal plasticity in cells expressing neuronal microtubule-associated proteins". ...
Karpova NN (January 2014). "Role of BDNF epigenetics in activity-dependent neuronal plasticity". Neuropharmacology. 76 Pt C: ... The gene early growth response protein 1 (EGR1) is an immediate early gene (IEG). EGR1 can rapidly be induced by neuronal ... Fernandes J, Arida RM, Gomez-Pinilla F (September 2017). "Physical exercise as an epigenetic modulator of brain plasticity and ... Duclot F, Kabbaj M (2017). "The Role of Early Growth Response 1 (EGR1) in Brain Plasticity and Neuropsychiatric Disorders". ...
June 2016). "Mitochondrial fusion/fission dynamics in neurodegeneration and neuronal plasticity". Neurobiology of Disease. 90: ... Boushel R, Lundby C, Qvortrup K, Sahlin K (October 2014). "Mitochondrial plasticity with exercise training and extreme ...
Mocchetti I (2005). "Exogenous gangliosides, neuronal plasticity and repair, and the neurotrophins". Cell Mol Life Sci. 62 (19- ... March 12, 2013). "Neuronal Expression of Glucosylceramide Synthase in Central Nervous System Regulates Body Weight and Energy ... and very low concentrations of a specific ganglioside can induce differentiation of cultured neuronal tumor cells. One NANA ("M ... where inadequate ganglioside expression in mediobasal hypothalamic neurons deregulates neuronal leptin and insulin signaling. " ...
In 2000, Shatz and colleagues identified Class I MHC molecules as important in neuronal plasticity, a surprising new role for ... Shatz, Carla J (2009). "MHC Class I: An Unexpected Role in Neuronal Plasticity". Neuron. 64 (1): 40-5. doi:10.1016/j.neuron. ... Goddard, C. A; Butts, D. A; Shatz, C. J (2007). "Regulation of CNS synapses by neuronal MHC class I". Proceedings of the ... Kanold, Patrick O; Kim, Yoon A; Grandpre, Tadzia; Shatz, Carla J (2009). "Co-regulation of ocular dominance plasticity and NMDA ...
The current through HCN channels, designated If or Ih, plays a key role in the control of cardiac and neuronal rhythmicity and ... This complexity is believed to affect neural plasticity. HCN channel was first identified in 1976 in the heart by Noma and ... H-current: properties of a neuronal and network pacemaker. Vol. 21. pp 9-12. Kaupp UB, Seifert R. Molecular diversity of ...
... has important physiological properties and impacts neuronal plasticity and repair mechanisms, and the release of ... Sphingolipidoses Structures of GM1, GM2, GM3 gangliosides Mocchetti I (2005). "Exogenous gangliosides, neuronal plasticity and ...
Memory and synaptic plasticity[edit]. Main article: Synaptic plasticity. Earlier models of memory are primarily based on the ... Chklovskii DB (2004). "Synaptic connectivity and neuronal morphology: two sides of the same coin". Neuron. 43 (5): 609-17. doi: ... Gerstner, W.; Kistler, W.; Naud, R.; Paninski, L. (2014). Neuronal Dynamics. Cambridge, UK: Cambridge University Press. ISBN ... Gerstner, W.; Kistler, W.; Naud, R.; Paninski, L. (2014). Neuronal Dynamics. Cambridge, UK: Cambridge University Press. ISBN ...
Collingridge GL, Isaac JT, Wang YT (2004). "Receptor trafficking and synaptic plasticity". Nat Rev Neurosci 5(12): 952-962, ... Eric Kandel was awarded the Nobel Prize in Physiology or Medicine for his research in neuronal learning processes. ...
The neuronal networks involved in respiratory function are located in the ventral respiratory column (VRC). From rostral to ... Plasticity of the mechanisms involved in respiratory behavior is modulated in part by the pre-Bötzinger complex. Disruption ... This single neuronal network can create multiple respiratory rhythmic patterns and is by itself both necessary and sufficient ... Neuronal discharge patterns are altered during the depressed synaptic inhibition, contributing to the reformation of the ...
Hence, greater transcriptome plasticity has come as the cost of slower genome evolution. High levels of RNA editing do not ... Editing is concentrated in the nervous system and affects proteins involved in neural excitability and neuronal morphology. ... "Trade-off between transcriptome plasticity and genome evolution in cephalopods". Cell. 169 (2): 191-202. doi:10.1016/j.cell. ...
It has been used not only in the study of neuronal plasticity and information processing but also in drug and toxin effects on ... Nevertheless, plasticity in neuronal networks is a phenomenon that is well-established in the neuroscience community, and one ... Researchers can then thoroughly study learning and plasticity in a realistic context, where the neuronal networks are able to ... The long timelines associated with studying neuronal plasticity (usually on the scale of months) makes extending the lifespan ...
There is some experimental evidence that RSK2 regulates synaptic transmission and plasticity in neuronal cell types.[3] ...
a b Demetriou, A., Spanoudis, G., & Mouyi, A. (2010). A Three-level Model of the Developing Mind: Functional and Neuronal ... Brain research shows that some general aspects of the brain, such as myelination, plasticity, and connectivity of neurons, are ... For example, increases in the myelination of neuronal axons, which protect the transmission of electrical signalling along the ... Demetriou, A., Spanoudis, G., & Mouyi, A. (2010). A Three-level Model of the Developing Mind: Functional and Neuronal ...
neuronal cell body. • perinuclear region of cytoplasm. • early endosome. • synaptic vesicle. • macromolecular complex. • ... regulation of synaptic plasticity. • negative regulation of epidermal growth factor-activated receptor activity. • cell ... Further study conducted in neuronal cultures derived from presenilin-1 deficient mouse embryos. They showed that cleavage by ...
Horton TH (Jan 2005). "Fetal origins of developmental plasticity: animal models of induced life history variation". Am. J. Hum ... resulting in particular heightened neuronal activity in response to stress-induced CRF release.[33] With repeated exposure to ... Macrì S, Würbel H (December 2006). "Developmental plasticity of HPA and fear responses in rats: a critical review of the ...
From Wolf et al. (2008): coping style, reactivity, flexibility, plasticity, and differential susceptibility. ... brain function and neuronal sensitization, and genetics.[7] For example, genetic studies provide evidence that higher levels of ... "Such differences in responsiveness (also termed coping style, reactivity, flexibility, plasticity) have been documented in many ... suggest increased plasticity (responsiveness) to both positive and negative influences; and the vantage sensitivity (VS) ...
Gengler S, Gault VA, Harriott P, Hölscher C (June 2007). "Impairments of hippocampal synaptic plasticity induced by aggregated ... o cal forma a base da excitotoxicidade neuronal. É unha opción para o tratamento de pacientes con enfermidade de Alzheimer de ... "Amyloid β-Protein Dimers Isolated Directly from Alzheimer Brains Impair Synaptic Plasticity and Memory". Nat. Med. 14 (8): 837 ...
Due to the plasticity of the human brain, the structure of its synapses and their resulting functions change throughout life.[ ... These questions include how signals are processed by neurites - thin extensions from a neuronal cell body, consisting of ... Computational neurogenetic modeling is concerned with the development of dynamic neuronal models for modeling brain functions ... neuronal migration, axonal and dendritic development, trophic interactions, and synapse formation. ...
When this repeat length exceeds 36, the onset of neuronal degradation and the physical symptoms of Huntington's can range from ... "HDAC2 negatively regulates memory formation and synaptic plasticity". primary. Nature. 459 (7243): 55-60. Bibcode:2009Natur. ... Sodium butyrate treatment slowed neuronal degeneration in Drosophila models.[18] Sodium butyrate treatment also increased ... Implications for selective neuronal vulnerability". primary. Neurobiology of Disease. 32 (3): 521-7. doi:10.1016/j.nbd.2008.09. ...
... found to be indistinguishable from control with respect to both neuronal death rates and measurements of synaptic plasticity.[ ... A possible role in regulating neuronal excitability". Neurosci. Lett. 103 (2): 139-44. doi:10.1016/0304-3940(89)90565-X. PMID ... Some research indicates PrP involvement in neuronal development, differentiation, and neurite outgrowth. The PrP-activated ... This effect can be positive or negative and is due to changes in neuronal excitability and synaptic transmission in the ...
2) ... It deaminates primary and secondary amines that are free in the neuronal cytoplasm but not those bound in storage ... Sabelli, HC; Mosnaim, AD; Vazquez, AJ; Giardina, WJ; Borison, RL; Pedemonte, WA (1976). "Biochemical plasticity of synaptic ... TAAR1 activity appears to depress monoamine transport and limit dopaminergic and serotonergic neuronal firing rates via ...
Mocchetti I (2005). "Exogenous gangliosides, neuronal plasticity and repair, and the neurotrophins". Cell. Mol. Life Sci. 62 ( ...
... eliminates the neuronal structural and plasticity effects caused by cocaine by means of this feedback which blocks ΔFosB ...
"Scaling of Brain Metabolism with a Fixed Energy Budget per Neuron: Implications for Neuronal Activity, Plasticity and ... "Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain". The Journal of ... with regard to numbers of neuronal and nonneuronal cells, the human brain is an isometrically scaled-up primate brain.. ... gross structural measures may not reflect functionally relevant factors such as neuronal connectivity and receptor density, and ...
Along with the fundamental behavioral studies, other work in the lab traced the neuronal circuits of sensory neurons, ... "Bidirectional regulation of hippocampal long-term synaptic plasticity and its influence on opposing forms of memory". J. ...
Inhibitory neurons using GABA, make compensating changes in the neuronal networks preventing runaway levels of excitation.[61] ... "Shaping inhibition: activity dependent structural plasticity of GABAergic synapses". Frontiers in Cellular Neuroscience. 8 ... Inhibitory neurons in the central nervous system play a homeostatic role in the balance of neuronal activity between excitation ...
... a novel neuronal PSD-95/SAP90-binding protein". The Journal of Biological Chemistry. 273 (41): 26269-72. doi:10.1074/jbc.273.41 ... and may be involved in the trafficking AMPAR during synaptic plasticity. ...
... of the granule cells and is thus said to be important in regulating neuronal development, neuronal plasticity, learning, and ... Plasticity of the synapse between a parallel fiber and a Purkinje cell is believed to be important for motor learning.[11] The ... Granule neurons have high levels of the neuronal isoform of nitric oxide synthase. This enzyme is dependent on the presence of ... These two populations of granule cells are also the only major neuronal populations that undergo adult neurogenesis, while ...
Phosphoinositides (PIP, PIP2, and PIP3) are molecules that have been shown to affect neuronal polarity.[12] A gene (ttx-7) was ... By altering the release of neurotransmitters, the plasticity of synapses can be controlled in the presynaptic cell. The ... Arimura, Nariko; Kaibuchi, Kozo (December 22, 2005). "Key regulators in neuronal polarity". Neuron. Cambridge, MA: Cell Press. ... Synapses are essential to neuronal function: neurons are cells that are specialized to pass signals to individual target cells ...
It may be related to oxidative stress, protein aggregation and neuronal death, but the mechanisms are not fully understood.[58] ... neural plasticity-principled approach to treating individuals with Parkinson disease and other neurological disorders". ... These brain sites are the main places of neuronal degeneration in PD; however, Lewy bodies may not cause cell death and they ...
Neural plasticity[edit]. NMDA receptors are also associated with synaptic plasticity. The idea that both synaptic and ... The GluN2B and GluN2A subunits also have differential roles in mediating excitotoxic neuronal death.[43] The developmental ... CDK5 regulates the amount of NR2B-containing NMDA receptors on the synaptic membrane, thus affecting synaptic plasticity.[95][ ... Memantine and newer derivatives could become very important weapons in the fight against neuronal damage.[15] ...
Ball, G.F.; Auger, C.J.; Bernard, D.J.; Charlier, T.D.; Sartor, J.J.; Riters, L.V.; Balthazart, J. (2004). "Seasonal plasticity ... "Support for a synaptic chain model of neuronal sequence generation". Nature. 468: 394-399. doi:10.1038/nature09514. PMC ... Brainard, M. S. & Doupe, A. J. (2000). "Interruption of a basal ganglia-forebrain circuit prevents plasticity of learned ... becomes highly expressed in Area X during periods of vocal plasticity in both juvenile zebra finches and adult canaries.[77] ...
The spike in neuronal activity correlating to this frequency is not restrained to the tonotopic organization of the auditory ... An evoked response study of congenitally deaf kittens used local field potentials to measure cortical plasticity in the ... Cant, NB; Benson, CG (June 15, 2003). "Parallel auditory pathways: projection patterns of the different neuronal populations in ... "The neuronal representation of pitch in primate auditory cortex". Nature. 436 (7054): 1161-5. Bibcode:2005Natur.436.1161B. doi ...
The neuronal networks underlying some of these oscillations are understood (e.g., the thalamocortical resonance underlying ... Anderson, Amy L; Thomason, Moriah E (2013-11-01). "Functional plasticity before the cradle: A review of neural functional ... A tutorial on analysis of ongoing, evoked, and induced neuronal activity: Power spectra, wavelet analysis, and coherence ... possibly because the normal and mirror neuronal systems "go out of sync" and interfere with one other.[78] ...
The chromatin landscape of neuronal plasticity.. Herre M1, Korb E2. ... Here, we review recent advances in chromatin regulation that contribute to synaptic plasticity and drive adaptive behaviors ... Examining the links between neuronal activity, transcriptional output, and synaptic function offers unique insights into how ...
... ranging from the basic neuronal machinery that implements synaptic and neuronal plasticity - i.e. elementary building blocks of ... Neuronal Plasticity, Learning, and Memory. Who we are as human individuals is determined to a large degree by the sum-total of ... Our multidisciplinary, multi-level experimental approach to neuronal plasticity, learning and memory encompasses a spectrum of ... systems that encode and store memory - to the concerted activity of neuronal circuits that encode and maintain experience- ...
... and has described three core CNS plasticity mechanisms. ... wrapping up neuronal plasticity" by Megan ORourke1, Robert ... Adult myelination -- Wrapping up neuronal plasticity. Neural Regeneration Research. Journal. Neural Regeneration Research. ... Adult myelination: wrapping up neuronal plasticity. Neural Regen Res. 2014;9(13):1261-1264. Contact: Meng Zhao [email protected] 86 ... much work remains to be done to determine whether synaptic plasticity, neurogenesis and myelin plasticity operate in a ...
Calmodulin-kinases: modulators of neuronal development and plasticity.. Wayman GA1, Lee YS, Tokumitsu H, Silva AJ, Soderling TR ... Neuronal Activity. Continued dendritic arborization (total length ,1000 μm) via neuronal activity requires Ca2+ influx through ... Neuronal activity, via Ca2+ influx through the NMDAR, can activate both CaMKII and CaMKK/CaMKI. (Left side) CaMKII is complexed ... Downstream targets of CaMKIα in this system remain to be identified-potential candidates are discussed in the text (Neuronal ...
TMS-induced neuronal plasticity enables targeted remodeling of visual cortical maps. Vladislav Kozyrev, Robert Staadt, Ulf T. ... TMS-induced neuronal plasticity enables targeted remodeling of visual cortical maps. Vladislav Kozyrev, Robert Staadt, Ulf T. ... TMS-induced neuronal plasticity enables targeted remodeling of visual cortical maps Message Subject (Your Name) has sent you a ... TMS-induced neuronal plasticity enables targeted remodeling of visual cortical maps. Vladislav Kozyrev, Robert Staadt, Ulf T. ...
Neural Plasticity publishes research and review articles from the entire range of relevant disciplines, including basic ... Open Access journal that publishes articles related to all aspects of neural plasticity, with special emphasis on its ... GABAergic Neuronal Precursor Grafting: Implications in Brain Regeneration and Plasticity. Manuel Alvarez Dolado1 and Vania ... To receive news and publication updates for Neural Plasticity, enter your email address in the box below. ...
... have shown that synaptic levels of the protein clathrin are a determinant factor for synaptic plasticity of neurons. ... The vesicular cycle must adapt to constant changes in neuronal activity, and thus is a determinant of neuronal plasticity. The ... researchers-discover-that-synaptic-levels-of-clathrin-protein-are-important-for-neuronal-plasticity ... Synaptic levels of clathrin protein are important for neuronal plasticity. IDIBELL-Bellvitge Biomedical Research Institute ...
... suggesting that it might be involved in neuronal plasticity [10].. *Persistent neuronal plasticity, including that observed at ... Methamphetamine-induced deficits of brain monoaminergic neuronal markers: distal axotomy or neuronal plasticity. Guilarte, T.R ... Methamphetamine-induced deficits of brain monoaminergic neuronal markers: distal axotomy or neuronal plasticity [38]. ... Apolipoprotein E and neuronal plasticity following experimental de-afferentation and in Alzheimers disease. Danik, M., Poirier ...
Neural Plasticity publishes research and review articles from the entire range of relevant disciplines, including basic ... Open Access journal that publishes articles related to all aspects of neural plasticity, with special emphasis on its ... Morphogenetic Plasticity of Neuronal Elements in Cerebellar Glomeruli during Deafferentation-Induced Synaptic Reorganization. ... József Hámori, Robert L. Jakab, and József Takács, "Morphogenetic Plasticity of Neuronal Elements in Cerebellar Glomeruli ...
... Neurobiol Dis. 2016 Jun;90:3-19. doi: ... Accordingly, inactivation of the main actors of mitochondrial fusion/fission dynamics is associated with defects in neuronal ... we present the central actors of mitochondrial fusion and fission and review the role of mitochondrial dynamics in neuronal ... development, plasticity and functioning, both ex vivo and in vivo. Here, ...
... ranging from changes in gene expression and epigenetic processes to aberrant synaptic plasticity to volumetric changes in ... ranging from changes in gene expression and epigenetic processes to aberrant synaptic plasticity to volumetric changes in ... ranging from changes in gene expression and epigenetic processes to aberrant synaptic plasticity to volumetric changes in ...
Synapse- and Stimulus-Specific Local Translation During Long-Term Neuronal Plasticity. By Dan Ohtan Wang, Sang Mok Kim, Yali ... Synapse- and Stimulus-Specific Local Translation During Long-Term Neuronal Plasticity. By Dan Ohtan Wang, Sang Mok Kim, Yali ... Synapse- and Stimulus-Specific Local Translation During Long-Term Neuronal Plasticity Message Subject. (Your Name) has ... To directly visualize translation at the level of individual synapses during long-term, learning-related neuronal plasticity, ...
Neuronal Activity and Adenylyl Cyclase in Environment-Dependent Plasticity of Axonal Outgrowth in Drosophila. Yi Zhong and Chun ... Neuronal Activity and Adenylyl Cyclase in Environment-Dependent Plasticity of Axonal Outgrowth in Drosophila ... Neuronal Activity and Adenylyl Cyclase in Environment-Dependent Plasticity of Axonal Outgrowth in Drosophila ... Neuronal Activity and Adenylyl Cyclase in Environment-Dependent Plasticity of Axonal Outgrowth in Drosophila ...
... J Neurochem ... to be the result of a cellular stress response that stimulates the production of proteins that enhance neuronal plasticity and ... The profound influences of the quantity and timing of food intake on neuronal function and vulnerability to disease have ... Moreover, DR can stimulate the production of new neurons from stem cells (neurogenesis) and can enhance synaptic plasticity, ...
A Novel Role for Protein Synthesis in Long-Term Neuronal Plasticity: Maintaining Reduced Postburst Afterhyperpolarization. ... We suggest that, much like synaptic plasticity, activity-induced long-lasting modulation of intrinsic neuronal excitability ... A Novel Role for Protein Synthesis in Long-Term Neuronal Plasticity: Maintaining Reduced Postburst Afterhyperpolarization ... A Novel Role for Protein Synthesis in Long-Term Neuronal Plasticity: Maintaining Reduced Postburst Afterhyperpolarization ...
Chan-Palay V. (1977) The Dynamic Nature of Neuron Connections: Neuronal Plasticity and Spontaneous Degeneration in the Normal ... The Dynamic Nature of Neuron Connections: Neuronal Plasticity and Spontaneous Degeneration in the Normal Cerebellum. ... A systematic analysis of this type begins with the definition of the most obvious neuronal elements-the perikarya of all ...
Rodent models of social stress and neuronal plasticity: relevance to depressive-like disorders.. Title. Rodent models of social ... Moderate to severe social stress appears to stimulate plasticity and neuronal growth in regions of the amygdala, whereas the ... Rodent models of social stress and neuronal plasticity: relevance to depressive-like disorders.. ... Rodent models of social stress and neuronal plasticity: relevance to depressive-like disorders. ...
Antibodies for proteins involved in positive regulation of long-term neuronal synaptic plasticity pathways, according to their ... Antibodies for proteins involved in positive regulation of long-term neuronal synaptic plasticity pathways; according to their ...
Shamma receives NIH grant to study spectro-temporal plasticity in the brains neuronal networks. Professor Shihab Shamma (ECE/ ... This kind of plasticity would likely involve a selective functional reshaping of the underlying cortical circuitry to sculpt ... They will extend studies of task-related plasticity in the auditory cortex to a variety of new tasks involving speech stimuli, ... lead to progress in understanding the interactions within an extended neuronal network that give rise to adaptive plasticity. ...
Understanding the signal filtering properties of this short-term plasticity (STP) is a challenge and requires theoretical ...
... to control neuronal development and plasticity. In spite of this important role, very little is known about additional proteins ... a useful starting point to investigate genes that interact with AP-1 in vivo to regulate neuronal development and plasticity. ... Screen in Drosophila Identifies Neuronal Roles of GSK-3β/shaggy as a Regulator of AP-1-Dependent Developmental Plasticity ... Overexpression Screen in Drosophila Identifies Neuronal Roles of GSK-3β/shaggy as a Regulator of AP-1-Dependent Developmental ...
Review Article: Phenotypic Plasticity of the Brain Neuronal networks and synaptic plasticity: understanding complex system ... Review Article: Phenotypic Plasticity of the Brain Neuronal networks and synaptic plasticity: understanding complex system ... Review Article: Phenotypic Plasticity of the Brain Neuronal networks and synaptic plasticity: understanding complex system ... Neuronal networks and synaptic plasticity: understanding complex system dynamics by interfacing neurons with silicon ...
Neuronal plasticity of human Whartons jelly mesenchymal stromal cells to the dopaminergic cell type compared with human bone ... Thus the focus of this study was to estimate the neuronal plasticity of WJ MSC to the dopaminergic (DA) cell type in comparison ... and the neuronal plasticity of human WJ MSC is comparable with that of BM MSC. ... For neuronal differentiation, MSC were exposed to developmentally relevant cues for midbrain DA neurons: sonic hedgehog (SHH) ...
Plasticity and stability in neuronal output via changes in intrinsic excitability: its whats inside that counts ... Plasticity and stability in neuronal output via changes in intrinsic excitability: its whats inside that counts ... Plasticity and stability in neuronal output via changes in intrinsic excitability: its whats inside that counts ... Plasticity and stability in neuronal output via changes in intrinsic excitability: its whats inside that counts ...
... neural plasticity; spike time dependent plasticity; spine motility; structural plasticity; time-lapse imaging. ... Mysore, Shreesh Pranesh (2007) Structural Plasticity in Neuronal Networks. Dissertation (Ph.D.), California Institute of ... Structural plasticity forms the focus of this thesis and motivates both the experimental and the computational modeling work ... Neuronal networks are established during development by the formation of connections (synapses) between neurons. Once formed, ...
Disease-associated mutations in Niemann-Pick type C1 alter ER calcium signaling and neuronal plasticity. Scott A. Tiscione, ... Disease-associated mutations in Niemann-Pick type C1 alter ER calcium signaling and neuronal plasticity ...
Activity-dependent plasticity of neuronal excitability a role for short-term modulation of voltage-gated ion channels in ... CHAPTER 2 Homeostatic scaling of neuronal excitability by synaptic modulation of somatic hyperpolarization-activated Ih ...
... Johansson, ... physiopathology, *Neuronal Plasticity, Rats, Inbred SHR, Support, Non-U.S. Govt. in Journal of Cerebral Blood Flow and ... Neuronal Plasticity,Rats,Inbred SHR,Support,Non-U.S. Govt}, language = {eng}, number = {1}, pages = {89--96}, publisher = { ... Neuronal plasticity and dendritic spines: effect of environmental enrichment on intact and postischemic rat brain.}, url = { ...
HIP/PAP prevents excitotoxic neuronal death and promotes plasticity Author(s) Haldipur, P. Dupuis, N. Degos, V. Moniaux, N. ... HIP/PAP prevents excitotoxic neuronal death and promotes plasticity. Haldipur, P, Dupuis, N, Degos, V, Moniaux, N, Chhor, V, ... HIP/PAP prevents excitotoxic neuronal death and promotes plasticity, Annals of Clinical and Translational Neurology, vol. 1, ... HIP/PAP prevented the formation of cortical and white matter lesions and reduced neuronal death and glial activation following ...
  • Examining the links between neuronal activity, transcriptional output, and synaptic function offers unique insights into how neurons adapt to changing environments and form memories. (
  • Here, we review recent advances in chromatin regulation that contribute to synaptic plasticity and drive adaptive behaviors through dynamic and precise regulation of transcription output in neurons. (
  • Researchers of the group of cellular and molecular neurobiology of the Bellvitge Biomedical Research Institute (IDIBELL) and the University of Barcelona, led by researcher Artur Llobet, have shown that synaptic levels of the protein clathrin are a determinant factor for synaptic plasticity of neurons. (
  • Moreover, DR can stimulate the production of new neurons from stem cells (neurogenesis) and can enhance synaptic plasticity, which may increase the ability of the brain to resist aging and restore function following injury. (
  • Learning-induced reduction in the postburst afterhyperpolarization (AHP), which results with enhanced neuronal excitability and decreased spike frequency adaptation, is apparent in hippocampal and cortical pyramidal neurons. (
  • Intense synaptic activation induces AHP reduction and enhanced neuronal excitability in hippocampal pyramidal neurons. (
  • While there has been extensive research to define the cellular and molecular basis of synaptic plasticity, at the level of either pairs of neurons or smaller networks, analysis of larger neuronal ensembles has proved technically challenging. (
  • Here we describe recent breakthroughs in the area of various bionic hybrids whereby neuronal networks have been successfully interfaced with silicon devices to monitor the output of synaptically connected neurons. (
  • This form of synaptic plasticity has been the main focus of neuroscience research over the past decade and has provided greater insights into both cellular and molecular mechanisms by which synapses between subsets of neurons can be altered. (
  • The network plasticity can be considered as the sum of individually summated synaptic changes that occur in groups of functionally related neurons. (
  • For neuronal differentiation, MSC were exposed to developmentally relevant cues for midbrain DA neurons: sonic hedgehog (SHH) and fibroblast growth factor 8 (FGF8), along with basic fibroblast growth factor (bFGF). (
  • We are only beginning to understand how neural networks strike a balance between altering individual neurons in the name of plasticity, while maintaining long-term stability in neural system function. (
  • Because of their fundamental role in generating neuronal output, it is not surprising that alterations in the properties, spatial distribution, or abundance of these ion channels can result in considerable plasticity for neurons and the networks to which they belong. (
  • Neuronal networks are established during development by the formation of connections (synapses) between neurons. (
  • Changes in the structure of synapses, neurons, and networks - collectively called structural plasticity - are the predominant mechanisms for changes in the network architecture in the brain. (
  • D1R-expressing (but not D2R) accumbal neurons also display reduced dendritic arborization (morphological plasticity), an important parameter in excitatory neurotransmission for the MSNs as dendritic spines are the primary site of excitatory synapses 8,10-12,19,20 . (
  • It is commonly thought that associative principles in neuronal networks should rely on correlations between the activity of neurons, which also must be somehow represented at the level of individual synapses", explains Júlia Gallinaro. (
  • Neuronal plasticity underpins learning and memory, but it is very challenging to tie changes in specific neurons to alterations in animal behavior,' explains Justin Blau, the paper's senior author and a professor in the New York University (NYU) Department of Biology and at NYU Abu Dhabi. (
  • In our research, we've discovered how plasticity of a very small number of neurons helps run the biological clock and aids transitions to different seasons. (
  • Estradiol rapidly modulates synaptic plasticity of hippocampal neurons: Involvement of kinase networks. (
  • Hypothalamic neurons respond to nutritional cues by altering gene expression and neuronal excitability. (
  • For proper neuronal network formation excitatory and inhibitory neurons as well as glia need to co-develop. (
  • Bioengineered Neuronal Organoids (BENOs) comprise interconnected excitatory and inhibitory neurons with supportive astrocytes and oligodendrocytes. (
  • These findings further our knowledge about the regulation of neuronal plasticity by astrocytes outside the neuron, as well as the regulation of plasticity from within the nuclei of the neurons themselves. (
  • show that homeostatic synaptic plasticity, the mechanism responsible for optimization of neuronal network activity, was abolished in human neurons generated from fragile X patient-derived induced pluripotent stem cells. (
  • Plasticity is the ability for the nervous system, more specifically neurons, and their synapses to modify their function and morphology due to experiences, which in turn correlate with changes in behavior. (
  • Although there is a decline in brain plasticity across lifespan, neurons in certain areas of the adult brain retain the ability to undergo synaptic, dendritic and spine remodeling in response to different stimuli. (
  • Moreover, recent evidences indicate that changes in the structure and connectivity of neurons in the mPFC may also underlie the pathogenesis of these diseases and that pharmacological treatments may revert these changes by enhancing the plasticity of neuronal connections. (
  • Although most of the studies on neuronal structural plasticity have been focused on principal neurons, there is abundant evidence that, in these psychiatric and neurological disorders, interneurons and cortical inhibitory networks show abnormalities. (
  • We are currently investigating whether Rac is an important molecule involved post-developmentally in synaptic plasticity in the adult mice, playing a role in the neuro-anatomical and cyto-architectural changes of neurons and in the activation of signal transduction pathways associated with LTP and hippocampal learning and memory. (
  • Memory performances were assessed in the Y-maze (n = 24-30/group), retinoic acid levels were measured (LC-MS/MS) in the serum and in the hippocampus (n = 5/group), CA1 neuronal architecture was analyzed with Golgi staining (n = 17-20 neurons/group) and electrophysiological patch-clamp recordings were performed on hippocampal brain slices (n = 6-11/group). (
  • Results: Vitamin A deficiency from weaning significantly lowered hippocampal levels of retinoic acid, reduced dendritic length and branching of CA1 pyramidal neurons and decreased spontaneous glutamatergic synaptic events and synaptic plasticity. (
  • Increasing evidence points to a neuro-modulatory role of cytokines and chemokines (CHEMOtactic cytoKINES) in basal transmission and plasticity processes where signaling between peri-synaptic astrocytes, microglia and neurons plays an important role. (
  • Manipulating H3.3 dynamics in both embryonic and adult neurons confirmed its essential role in neuronal plasticity and cognition. (
  • Recently, we have deleted Brg1 specifically in neurons and discovered that Brg1 is required for synapse development and MEF2-mediated activity-induced gene expression and synapse plasticity. (
  • They are highly 'plastic', changing the way they transmit information between neurons in response to specific patterns of neuronal activity. (
  • Although multiple neurons can receive a stimulus, only a subset of the neurons will induce the necessary plasticity for memory encoding. (
  • The selection of this subset of neurons is termed neuronal allocation. (
  • Neuronal allocation is a phenomenon that accounts for how specific neurons in a network, and not others that receive similar input, are committed to storing a specific memory. (
  • The investigations focus on the neural plasticity found in the rodent hippocampal formation, referred to as long-term potentiation or enhancement (LTE), that may reflect processes normally involved in information storage in the brain. (
  • Whole-cell recording from a hippocampal slice Neuroinflammation is a hallmark of almost every neurological disorder, from acute head injury and stroke to most neurodegenerative diseases, and is thought to be a major contributor to the disruption of neuronal function and cell death.However, it remains unclear how the inflammation, driven by the release of pro-inflammatory cytokines, is contributing to the damage. (
  • It was further thought that there would be coincident increases in neuronal activity in hippocampal slices and increased expression of genes modulating neuronal excitability. (
  • In addition, mice lacking IL-6 have improved cognitive functions whereas the absence of microglia-driven CX3CR1 signaling increases hippocampal plasticity and spatial memory occluding the potentiating effects of EE. (
  • Interestingly, it has been suggested that chemokines can play a key role in the flexibility of hippocampal structure and may modulate neuronal signaling during behavior. (
  • Long-term potentiation (LTP) in hippocampal neuronal cultures induced ADAM10 endocytosis through AP2 association and decreased surface ADAM10 levels and activity. (
  • Thus, highly regulated local translation occurs at synapses during long-term plasticity and requires trans-synaptic signals. (
  • One mechanism that has been proposed to mediate this spatial restriction of gene expression during neuronal plasticity involves regulated translation of localized mRNAs at stimulated synapses ( 8 - 10 ). (
  • However, direct evidence that a specific mRNA undergoes spatially restricted translation at stimulated synapses during transcription-dependent synaptic plasticity has been lacking. (
  • To directly visualize translation at the level of individual synapses during long-term, learning-related neuronal plasticity, we used the Aplysia sensory neuron (SN)-motor neuron (MN) culture system ( 2 ). (
  • Once formed, these synapses undergo experience-dependent modifications throughout the lifespan of the animal (synaptic plasticity). (
  • In the mature brain, CS is concentrated in perineuronal nets (PNNs), which are extracellular structures that surround synapses and regulate synaptic plasticity. (
  • The NMDA receptor and mGluR5 are important mediators of synaptic plasticity - the ability of synapses to change their strength in response to changed patterns of neuronal activity. (
  • Mf-CA3 synapses are large synapses with multiple release sites and are characterized by a large dynamic range of presynaptic plasticity 16 . (
  • There is general agreement that homeostatic synaptic plasticity can be global (uniform scaling across all synapses of a neuron) or local (synaptic strength not uniformly scaled), and can be mediated by diverse molecular mechanisms. (
  • Synaptic plasticity is generally believed to be a result, at least in part, from the alteration in the number of AMPA-type glutamate receptors found at excitatory synapses. (
  • Homeostatic synaptic plasticity entails the uniform adjustments in the strength of all synapses on a given cell in response to prolonged changes in the cell's electrical activity, and is critical for the stability of neuronal circuits. (
  • It is of great interest to understand the mechanism that lead to lose of synapses and defective synaptic plasticity. (
  • IEG proteins can directly modify synapses and provide insight into cellular mechanisms that support synapse-specific plasticity. (
  • Our overarching interest is in the questions of how synapses find the right balance between plasticity and stability, and how alterations in this delicate equilibrium contribute to neurological disorders. (
  • In mature synapses, they regulate structural and functional synaptic plasticity by signaling between the two sides of the synapse. (
  • Newly generated plasticity-related proteins (PRPs) can be captured by any tagged synapses, but untagged synapses are not eligible to receive new PPs. (
  • Intense research over the last 25 years has provided critical insight into the cell generation and differentiation potential of endogenous neural stem and progenitor cells, and has described three core CNS plasticity mechanisms. (
  • While we are still a long way from fully understanding how neural plasticity is regulated from the level of the individual cell, through to the level of the neural network, there is growing evidence to support the idea that neurogenesis, synaptogenesis and myelin remodelling dynamically and co-operatively alter the structure and function of neural circuits in the adult CNS. (
  • While new genetic and imaging tools have led to major advances in our understanding of each plasticity mechanism separately, much work remains to be done to determine whether synaptic plasticity, neurogenesis and myelin plasticity operate in a coordinated and synergistic manner, as we have proposed, to regulate neural networks and support functions such as learning and memory, which span multiple CNS regions. (
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  • Manuel Alvarez Dolado and Vania Broccoli, "GABAergic Neuronal Precursor Grafting: Implications in Brain Regeneration and Plasticity," Neural Plasticity , vol. 2011, Article ID 384216, 11 pages, 2011. (
  • József Hámori, Robert L. Jakab, and József Takács, "Morphogenetic Plasticity of Neuronal Elements in Cerebellar Glomeruli during Deafferentation-Induced Synaptic Reorganization," Journal of Neural Transplantation and Plasticity , vol. 6, no. 1, pp. 11-20, 1997. (
  • These genetic alterations are thought to perturb mechanisms relevant to activity-dependent neural plasticity, in which neuronal activity activates the cAMP pathway, and consequently affect nerve terminal arborization by regulating expression of adhesion molecules. (
  • The balance of this plasticity and stability in neural networks undoubtedly plays a critical role in the normal functioning of the nervous system. (
  • While mechanisms of synaptic plasticity have garnered extensive study over the past three decades, it is only recently that more attention has been turned to plasticity of intrinsic excitability as a key player in neural network function. (
  • Thus mechanisms that alter neuronal excitability can lead to plasticity in responses to synaptic stimulation, ultimately affecting processes such as learning and memory and other activity-dependent forms of neural plasticity. (
  • Taken together, our work argues that architectural changes are a powerful and indispensable form of neural plasticity and sheds new light on the mechanisms of structural plasticity in the brain, thereby contributing to our understanding of learning and memory. (
  • More importantly, how do these mechanisms of plasticity integrate with ongoing mechanisms of regulation of neural intrinsic excitability and, in turn, homeostasis of entire neural circuits? (
  • It is important to note that this is the first time that the cooperativity between different isoforms of protein kinase C (PKC) have been shown to play a role in graded long-term change in neuronal activity and, in turn, providing the neural basis of species-specific behavior. (
  • They used methods from computational neuroscience and performed large-scale simulations of spiking neural networks with a structural plasticity rule based on firing rate homeostasis. (
  • 1989). These data suggest the exciting possibility that transcription factor genes may regulate other proteins that play a critical role in the maintenance of neural plasticity in brain. (
  • The biological evidence of neural plasticity implies revisiting the notion of determinism, in general as well as in the psychological dimension. (
  • Engulfment of neuronal cell bodies and fragments is critical for neural health and proper circuit connectivity. (
  • Among the numerous candidate molecules that have been identified for mediating this neuronal remodeling, cell adhesion molecules and, specially, the neural cell adhesion molecule (NCAM), are of particular interest. (
  • Thus, rapid de novo transcription provides novel insights into the cellular and neural network basis of behavioral plasticity. (
  • The goal of this project is to provide mechanistic insights on how the interplay between integrins and glutamate receptors alters neuronal circuits in autism and depression, and to develop treatments for 'opening a window' of persistent structural normalization of neural circuitries in these pathologies. (
  • This `homeostatic plasticity' has more recently been implicated as a mechanism of stabilizing neuronal function. (
  • It is these three aspects of plasticity in neuronal excitability in mature nervous systems that will be discussed in this review: long-term potentiation and depression of intrinsic excitability, homeostatic plasticity of neuronal excitability, and changes in excitability following perturbation of afferent input. (
  • February 20, 2018: Scientists from the Bernstein Center Freiburg demonstrated that Hebbian association in neuronal networks can also emerge from homeostatic plasticity, which is normally thought to exclusively stabilize neuronal activity. (
  • Similar to learning rules which explicitly depend on correlations, homeostatic plasticity implements some sort of "social networking" in the brain. (
  • We can now probe the role of TNFα and homeostatic plasticity in the nervous system. (
  • Removing TNFα signaling interferes with the ocular dominance plasticity observed in the visual cortex following monocular deprivation, suggesting a role for homeostatic plasticity in this process. (
  • TNFα-dependent homeostatic plasticity defines an intrinsic neuronal function for a pro-inflammatory signaling molecule and suggests that immune signaling molecules serve novel functions in the normal functioning of the nervous system. (
  • As postdoctoral fellow, he specialized in synaptic physiology in the laboratory of Dr. Yukiko Goda at the MRC Laboratory for Molecular Cell Biology (University College London), where he uncovered the role of cell adhesion in homeostatic plasticity. (
  • In neuropsychiatric disorders like depression structural remodeling involves apoptosis, reduced neurogenesis, and structural remodeling of neuronal dendrites which most likely reflects the latter. (
  • It provides an extensive overview of the latest insights in the role of sleep in regulating gene expression, synaptic plasticity and neurogenesis and how that in turn is linked to learning and memory processes. (
  • Indeed exposure of mice to environmental enrichment (EE) modifies learning and memory abilities increasing neurogenesis and neuronal plasticity whether exposure to severe stressful experiences diminishes neurotrophic support, impairs neurogenesis, plasticity and cognition. (
  • We show that high-frequency TMS creates a transient cortical state with increased excitability and increased response variability, which opens a time window for enhanced plasticity. (
  • This kind of plasticity would likely involve a selective functional reshaping of the underlying cortical circuitry to sculpt the most effective receptive field for accomplishing the current auditory task. (
  • They will explore plasticity in higher-order auditory cortical fields, and investigate the possible role of top-down signals from frontal cortex in modulating adaptive plasticity in the auditory cortex. (
  • HIP/PAP prevented the formation of cortical and white matter lesions and reduced neuronal death and glial activation following excitotoxic insults in vivo. (
  • Cortical development is a tightly regulated process that involves progenitor proliferation, neuronal differentiation and migration, programed cell death, and circuit formation. (
  • Role of cortical interneurons and plasticity-related molecules. (
  • We produced T1 knockout mice (KO), which show extensive axon regeneration following spinal cord injury, as well as the loss of onset of ocular dominance plasticity. (
  • T1KO loses the opening of ocular dominance plasticity. (
  • Ocular dominance plasticity is a model of activity-dependent plasticity in the visual cortex that has been extensively used to investigate the mechanisms underlying neuronal plasticity. (
  • My results reveal that the astrocyte-secreted, trans-synaptic bridging protein hevin, as well as three nuclear transcription factors CREB, SRF and MEF2, are indispensable to ocular dominance plasticity. (
  • Additionally, I found that the activation of CREB via phosphorylation at serine 142 and 143 is required for ocular dominance plasticity. (
  • Our multidisciplinary, multi-level experimental approach to neuronal plasticity, learning and memory encompasses a spectrum of cutting-edge methods, ranging from state-of-the-art molecular biology and electrophysiology in animal models to sophisticated psychophysics and behavior, modeling, and the most advanced behavioral protocols and functional neuroimaging of the behaving human brain. (
  • With experiments, we look in detail at one form of structural plasticity, namely dendritic spine dynamics. (
  • Neuronal plasticity and dendritic spines: effect of environmental enrichment on intact and postischemic rat brain. (
  • These data implicate RhoB in cofilin regulation and dendritic and spine morphology, highlighting its importance in synaptic plasticity at a structural and functional level. (
  • CREB modulates cellular processes that lead to neuronal allocation, particularly with regards to dendritic spine density and morphology. (
  • This lecture 1/15 is part of the Computational Modeling of Neuronal Plasticity Course that aims to teach users how to build a mathematical model of a neuron, its inputs, and its neuronal plasticity mechanisms, by writing your own Python program. (
  • Homeostatic regulation of excitability and synaptic efficacy works in conjunction with acutely induced Hebbian plasticity to maintain neuron firing within limits and thus preserve network stability and information flow. (
  • Vital investigation of genome activity and its role in mechanisms of long-term synaptic plasticity formation were studied in LP11 neuron (command neurone of defence behaviour) during sensitisation (simple form of learning) in semi-intact preparation of snail Helix lucorum. (
  • Metaplasticity is a term describing the likelihood that a given stimulus will induce neuronal plasticity, based on the previous activity experienced by that neuron. (
  • Thus, our laboratory is investigating Rac-dependent regulation of neuronal morphology in syndromes presenting impaired cognition. (
  • This review summarizes key neuronal functions of the CaMK cascade in signal transduction, gene transcription, synaptic development and plasticity, and behavior. (
  • The monosynaptic connection formed between SNs and MNs, a central component of the gill-withdrawal reflex in Aplysia , can be reconstituted in culture, where well-characterized stimuli elicit forms of plasticity that have direct correlates in the behavior of the animal. (
  • These advances have not yet, however, resolved the attributes of network plasticity, nor have they elucidated the cellular basis of any given behavior - owing primarily to our inability to monitor direct cellular activity at the level of larger neuronal ensembles. (
  • This is true for any biochemical activity that accompanies neuronal functional activity and accompanies behavior. (
  • 2) Experiments designed to determine whether there are changes in regulation of transcription factor activation in old animals that may contribute to their altered synaptic plasticity and behavior. (
  • The contribution of astrocytes and oligodendrocytes to neuronal plasticity and behavior has expanded vastly in recent years. (
  • moreover negative effects on neuronal plasticity (and thus behavior) induced by stress exposure can be prevented by blocking IL-1 activity. (
  • However, the factors mediating the effect of environmental stimuli on behavior and plasticity has been only partially identified. (
  • Since some forms of spinocerebellar ataxia are associated with mutations in human Puratrophin-1, our data support the idea that defective neuronal plasticity underlies loss of motor control and leads to neurodegeneration,' notes Blau. (
  • The receptor trafficking induced by TNFα underlies homeostatic synaptic plasticity. (
  • This plasticity underlies every event of learning and memory that is crucial to our daily lives. (
  • Since spinocerebellar ataxia is associated with mutations in human Puratrophin-1, our data support the idea that defective actin-related plasticity underlies this ataxia. (
  • Short-term modulation of intrinsic neuronal excitability can be also induced in vitro . (
  • We suggest that, much like synaptic plasticity, activity-induced long-lasting modulation of intrinsic neuronal excitability requires molecular consolidation. (
  • Thus, the question arises whether protein synthesis inhibitors affect memory consolidation via additional neuronal processes, such as modification and maintenance of neuronal excitability. (
  • Neuronal excitability is directly attributable to the suite of ion channels inserted into the membrane of the cell, as well as the biochemical properties and kinetics of those channels. (
  • Plasticity in intrinsic excitability may play multiple important roles in the functioning nervous system. (
  • Examples of plasticity in intrinsic neuronal excitability. (
  • Using computational approach, we observed that altered intrinsic excitability in the FSINs could massively impact the network activities and the effect was dependent on the cause of the plasticity. (
  • In some experiments one particular variant- p38g -is correlated with less neuronal excitability and induced seizures. (
  • At the neuronal level, cells with higher levels of excitability (for example lower slow afterhyperpolarization) are more likely to be recruited into a memory trace, and substantial evidence exists implicating the cellular transcription factor CREB (cyclic AMP responsive element-binding protein) in this process. (
  • In short," said Llobet "we showed that clathrin levels are a limiting factor for synaptic transmission, thus contributes to synaptic plasticity. (
  • Accordingly, the roles of both PS and APP in synaptic transmission and plasticity have been studied in several cellular and mouse models (reviewed in ref. 8 for PS and in ref. 9 for APP). (
  • The excitatory corticostriatal pathway, which plays a critical role in the building up and storage of adaptive motor behaviours, can undergo long-lasting, activity-dependent changes in the efficacy of synaptic transmission, named long-term potentiation (LTP) and long- term depression (LTD). Both forms of plasticity are thought to underlie motor learning and depend upon the concomitant activation of glutamatergic corticostriatal and dopaminergic nigrostriatal pathways. (
  • Calmodulin-kinases: modulators of neuronal development and plasticity. (
  • AP-1, an immediate-early transcription factor comprising heterodimers of the Fos and Jun proteins, has been shown in several animal models, including Drosophila, to control neuronal development and plasticity. (
  • Other candidates identified in this screen provide a useful starting point to investigate genes that interact with AP-1 in vivo to regulate neuronal development and plasticity. (
  • Drugs of abuse induce a host of alterations in brain structure and function, ranging from changes in gene expression and epigenetic processes to aberrant synaptic plasticity to volumetric changes in discrete brain regions. (
  • First, all of the machinery required for translation is present in neuronal processes, including polyribosomes ( 11 , 12 ), translation factors ( 13 ), and a select population of mRNAs ( 14 - 18 ). (
  • Plasticity processes are generally thought to come in two flavors: Hebbian or homeostatic. (
  • N-Methyl- D -Aspartate Receptor (NMDAR) are ubiquitously expressed along the central nervous system and are instrumental to various physiological processes such as synaptic plasticity and learning. (
  • The N-Methyl- D -Aspartate receptors (NMDAR) are members of the iGluR superfamily and are pivotal to many physiological processes such as the formation of long term memory, synaptic plasticity and many other cognitive functions. (
  • This neuronal structural plasticity seems to be the basis for many cognitive processes and it is crucial for adaptive responses to aversive experiences and recovery from brain damage and disease. (
  • Nevertheless, the exact mechanisms as to how cytokines, and in particular chemokines, participate in the molecular and cellular processes thought to subserve memory formation, plasticity processes and responsiveness to environmental stimuli remain to be clarified. (
  • For this reason, the main objectives of this thesis are to study the influence of dopaminergic neurotransmission on the neuronal plasticity of prefrontocortical circuits and to evaluate whether changes in the expression of PSA-NCAM are responsible for these neuroplastic changes. (
  • The goal of this project is to provide mechanistic insights on how the interplay between cell adhesion molecules (integrins) and glutamate receptors alters key neuronal circuits in autism. (
  • Our laboratory specialises on the technical development and application of light- and genetics-based functional imaging approaches to understand how behaviour emerges from the electrical activities of neuronal circuits. (
  • Long-term memory and synaptic plasticity require changes in gene expression and yet can occur in a synapse-specific manner. (
  • In this regard, there is evidence pointing to the Rho family of small GTPases, proteins that mediate actin cytoskeleton reorganization, neuronal morphogenesis and gene expression. (
  • Despite such accumulation, H3.3-containing nucleosomes remain highly dynamic-in a modification-independent manner-to control neuronal- and glial-specific gene expression patterns throughout life. (
  • Arc is an immediate early gene involved in synaptic plasticity, learning and memory. (
  • We are investigating how chromatin remodeling factors are recruited to specific target gene sites and how they response to neuronal calcium signaling to activate gene expression during synapse development and maturation. (
  • The vesicular cycle must adapt to constant changes in neuronal activity, and thus is a determinant of neuronal plasticity. (
  • The work, which appears in the journal Cell , focuses on the regulation of 'neuronal plasticity'--changes in neuronal structure--and its function in the brain. (
  • Understanding such changes in neuronal plasticity may have an impact on therapeutic strategies for memory disorders in both normal and pathological conditions of aging. (
  • We have in this work studied the plasticity of neuronal glutamate receptors and how novel accessory proteins can modulate their calcium mobilization. (
  • Taken together, our studies will clarify the homeostatic functions of key signaling proteins and offer a fresh approach to the possible links between the abnormal homeostatic adaptation and neuronal disorders like ASD. (
  • Identifying the specific proteins involved in these mechanisms is the first step to finding viable therapeutic targets in disorders like Fragile X syndrome, autism spectrum disorder and major depressive disorder, where plasticity is disrupted. (
  • modifications in intrinsic neuronal properties also subserve learning-related behavioral changes. (
  • Here we review key findings from animal models of psychosocial stress that have been used to gain insights into the relation between stress-related behavioral disorders like depression and structural plasticity. (
  • The exact form of this plasticity depends on the behavioral context, and the spectrotemporal features of the salient acoustic stimuli. (
  • They will extend studies of task-related plasticity in the auditory cortex to a variety of new tasks involving speech stimuli, new behavioral paradigms (contrasting discrimination versus recognition). (
  • Mice lacking Norbin displayed decreased cell surface expression of mGluR5, impaired synaptic plasticity, and a behavioral phenotype that corresponds to hypofunctional mGluR5 activity. (
  • The question is how cytokines may translate environmental stimuli in plasticity and behavioral changes. (
  • They will also test the idea that top-down influences from frontal areas contribute to the induction of rapid adaptive plasticity in the auditory cortex during auditory tasks, reflecting both the nature of the stimuli and goals of the tasks. (
  • Unlike other lncRNAs, the induction of eRNA is rapid and transient, and tightly regulated by external stimuli such as neuronal activity. (
  • In particular, an answer to the question of how the relatively unspecific nature of TMS stimulation leads to specific neuronal reorganization, as well as a detailed picture of TMS-triggered reorganization of functional brain modules, is missing. (
  • Our study," adds the researcher "questions this dogma because we found that in periods of intense neuronal stimulation, but within physiological levels, presynaptic levels of clathrin decrease reversibly. (
  • Here, we present the central actors of mitochondrial fusion and fission and review the role of mitochondrial dynamics in neuronal physiology and pathophysiology. (
  • Overexpression of Serum Response Factor in Astrocytes Improves Neuronal Plasticity in a Model of Fetal Alcohol Spectrum Disorders. (
  • Preliminary studies from simultaneous neuronal recordings of single units and local field potentials in the auditory and frontal cortex have already led to exciting new insights, and may lead to progress in understanding the interactions within an extended neuronal network that give rise to adaptive plasticity. (
  • The role of the small GTPases-linked genes could provide a connection between the mechanism and the neuronal microstructural deficits observed in these cognitive disorders. (
  • In this form of plasticity, either the amount of neurotransmitter released from the presynaptic terminal or its receptor function in the postsynaptic cell is modulated. (
  • Findings suggest that early life working memory training regulates shifts in neuronal morphology following neonatal brain injury. (
  • Such structural changes underlying long-term plasticity are more permanent, require longer time periods to develop and are contingent upon de novo protein synthesis. (
  • The neuronal MPS contains molecules homologous to the components of the erythrocyte membrane skeleton ( Bennett and Baines, 2001 ) but adopts a different ultrastructural organization. (
  • As postdoctoral fellow, he joined the laboratory of Dr. Yukiko Goda at the MRC Laboratory for Molecular Cell Biology (University College London), where he studied the relationship between synaptic structure and function, uncovering the role of cell adhesion molecules in homeostatic synaptic plasticity. (
  • Synaptic activity can generate a synaptic tag, which is a marker that allows the stimulated spine to subsequently capture newly transcribed plasticity molecules such as Arc. (
  • 40 day BENO indicate progressive neuronal network maturation. (
  • As financial, with the free Maturation Phenomenon in Cerebral Ischemia II: Neuronal Recovery of materials Auriea Harvey and Michael Samyn, there provides no graphical Y to interact derived, or is to date set. (
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  • The buy Maturation Phenomenon in Cerebral Ischemia II: Neuronal Recovery and Plasticity 1997 proposes the integrated conclusions from letters infected in shape. (
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  • Indeed, through the mechanisms of plasticity, experience leaves a trace in the neuronal network. (
  • The profound influences of the quantity and timing of food intake on neuronal function and vulnerability to disease have revealed novel molecular and cellular mechanisms whereby diet affects the nervous system, and are leading to novel preventative and therapeutic approaches for neurodegenerative disorders. (
  • This minisymposium will uncover recent evidence demonstrating the dynamic role of neuronal populations in the development of functional neocortical ensembles and highlight the cellular hubs of disease-related miswiring. (
  • This symposium will showcase the cellular infrastructure that supports neuronal development, stability and plasticity. (
  • To understand the genomic basis of phenotypic plasticity, the description of the precedent cellular and neuronal mechanisms is fundamental. (
  • These results from T1KO mice suggest important roles for extracellular CS in the brain regarding neuronal plasticity and axon regeneration. (
  • Neuronal networks in the brain undergo steady remodeling. (
  • Steroids in the brain: regulators of brain plasticity and protectors against neuronal damage. (
  • article{Beyer2012SteroidsIT, title={Steroids in the brain: regulators of brain plasticity and protectors against neuronal damage. (
  • Hyper-connectivity and hyper-plasticity in the prefrontal cortex implies hyper-functionality of one of the highest order processing regions in the brain, and stands in contrast to the hypo-functionality that is normally proposed in this region to explain some of the autistic symptoms. (
  • This book discusses a particular aspect of brain function, that of storage and retrieval of memory of past experience, in terms of neuronal plasticity. (
  • Simultaneously, TNFα also regulates neuronal inhibition, by causing an endocytosis of the GABA-A receptor, the principle mediator of fast inhibition in the brain. (
  • The similarity of structural and functional properties to the fetal brain may allow for the application of BENOs in studies of neuronal plasticity and modeling of disease. (
  • Activity-dependent neuronal plasticity is an essential process for the brain to change in response to its surroundings, both during development and in adulthood. (
  • Despite decades of research, we have yet to understand how the brain coordinates plasticity mechanisms to adapt to constantly changing environmental conditions. (
  • Neuronal plasticity due to early sensory or learning experience has been suggested to facilitate recovery of function after neonatal brain injury. (
  • In consonance with this fact, PSA-NCAM expression, which is very high during brain development, is only retained in adult brain regions that display a high degree of neuronal structural plasticity. (
  • This research topic is proposed to explore the role of cytokines, and more in particular chemokines, in the modulation of neuronal activity as a fundamental step for the correct brain wiring, function and susceptibility to environment. (
  • Although axonal impairment has long been known to be devastating for brain function in disease, until recently it was thought that axons showed minimal plasticity in healthy brains. (
  • This symposium will highlight recent advances in mechanisms controlling axonal function, how these mechanisms are plastic, and how axonal plasticity impacts brain function. (
  • Our findings establish histone turnover as a critical and previously undocumented regulator of cell type-specific transcription and plasticity in mammalian brain. (
  • Research in Cho group focuses on a wide range of projects from molecular mechanisms of synaptic plasticity in the brain to pathological aspects of the central nervous system (CNS) including Alzheimer's disease. (
  • However, we do not know how this richness influences brain function and synaptic plasticity. (
  • Increasing brain plasticity after stroke represents an important alternative strategy. (
  • Alternatively, the phenomenon of increasing brain plasticity after stroke provoke an essential therapy. (
  • Moreover, the study revealed that the FSIN membrane potential could modulate the expression of the plasticity. (
  • All neuronal and endocrine stimulants were able to modulate but not induce defences, indicating a pathway of interlinked steps. (
  • Neuronal activity, via Ca 2+ influx through the NMDAR, can activate both CaMKII and CaMKK/CaMKI. (
  • Analysis of ion channel and cAMP pathway mutants indicates that this temperature-dependent plasticity is mediated via neuronal activity changes linked to mechanisms controlled by the rutabaga -encoded adenylyl cyclase. (
  • Analysis of ion channel and cAMP pathway mutants reveals that this temperature-dependent plasticity is mediated by neuronal activity changes. (
  • There is an optimal level of neuronal activity at which nerve terminals will show the highest degree of ramification. (
  • This neuronal activity change was linked to nerve terminal arborization via mechanisms controlled by the rutabaga ( rut )-encoded adenylyl cyclase. (
  • Additionally, the connectivity pattern itself can be modified in an activity-dependent manner (architectural plasticity). (
  • Morphological plasticity of spines accompanies activity-dependent changes in synaptic strength. (
  • Homeostatic regulation of connectivity, in contrast, is thought to mainly stabilize neuronal signaling and network wiring to avoid runaway activity and unbounded growth. (
  • Júlia Gallinaro and Stefan Rotter could show that such specific connectivity can indeed emerge in a network which is continuously remodeled using a structural plasticity rule that does not explicitly depend on activity correlation. (
  • Synaptic plasticity is one of the fundamental characteristics of the nervous systems, and is thought to underlie learning and memory, including aberrant forms of learning such as drug addiction and neuropathic pain, as well as the activity-dependent refinement of connectivity observed during development. (
  • Moreover, the TNFα is of glial origin, suggesting glia detect neuronal activity and feedback homeostatic signals, including TNFα. (
  • I used in vivo electrophysiology as well as microscopy and biochemistry techniques to identify novel players in activity-dependent plasticity in the visual cortex. (
  • Function of chromatin remodeling complexes in neuronal activity-dependent transcription and synapse plasticity. (
  • Our findings will provide novel insight into the neuronal reorganization that takes place post-injury, which is needed if patients with peripheral nerve and central spinal deafferentation injuries are to be treated more effectively. (
  • Study investigators have sought to determine the role of clathrin in synaptic plasticity. (
  • Second, studies using protein synthesis inhibitors indicate a central role for local translation during long-lasting synaptic plasticity ( 5 , 19 , 20 ). (
  • We are interested in exploring other role for this form of plasticity in nervous system function. (
  • D2R agonist-induced increases in GAD67 and SYN neuropil expression were blocked when PSA was previously removed, indicating a role for PSA-NCAM in this plasticity. (
  • These data demonstrate structural plasticity of the MPS and suggest its potential role in early steps of axon degeneration. (
  • In the hippocampus cytokines play a key role in mediating both positive as well as negative effects of the environment affecting neuronal plasticity also in stress related pathologies, such as depression. (
  • The local fast-spiking interneurons (FSINs) are considered to be crucial for the generation, maintenance and modulation of neuronal network oscillations especially in the gamma frequency band. (
  • Induction of neuronal plasticity during adulthood. (
  • In contrast, α2δ2 pharmacological blockade through gabapentin administration promoted corticospinal structural plasticity and regeneration in adulthood. (
  • The principles of neuroscience and those of clinical practice, in the particular from the psychoanalytical angle, can meet in our view around a series of critical questions such as that of neuronal plasticity (Ansermet and Magistretti 2007). (
  • Endocytosis of synaptic ADAM10 in neuronal plasticity and Alzheimer's disease. (
  • Human LilrB2 is a Beta-Amyloid Receptor and its Murine Homolog PirB Regulates Synaptic Plasticity in an Alzheimer's Model , Kim, T et al. (
  • Indeed, Sano and colleagues in the Silva lab showed that CREB also regulates neuronal memory allocation in the amygdala. (
  • The waterflea Daphnia is a model to investigate the genetic basis of phenotypic plasticity resulting from one differentially expressed genome. (
  • In conclusion, dopamine is suggested as a key regulator of phenotypic plasticity. (
  • We demonstrated that increasing the rearing temperature enhances motor nerve terminal arborization, indicating that nerve terminal plasticity observed in this model preparation is not merely an abnormal phenotype that is only seen in mutants but a natural mechanism for adaptation to environmental changes. (
  • The transcription factor cAMP response element-binding protein (CREB) is a well-studied mechanism of neuronal memory allocation. (
  • One member of this family, CaMKII, is well-established for its effects on modulating synaptic plasticity and learning and memory. (
  • rather it exhibits a high degree of plasticity, which in turn forms the basis for learning and memory. (
  • These technologies hold tremendous potential for future research not only in the area of synaptic plasticity but also for the development of strategies that will enable implantation of electronic devices in live animals during various memory tasks. (
  • In this study, we characterized the impact of vitamin A deficiency on memory and neuronal plasticity, focusing on the CA1 region of the hippocampus in rats. (