Pyramidal Cells
Hippocampus
Interneurons
Dendrites
Excitatory Postsynaptic Potentials
Synapses
Action Potentials
Neocortex
CA3 Region, Hippocampal
CA1 Region, Hippocampal
Neural Inhibition
Synaptic Transmission
Patch-Clamp Techniques
Rats, Sprague-Dawley
Mossy Fibers, Hippocampal
Neurons
Electrophysiology
Pyramidal Tracts
Theta Rhythm
Models, Neurological
Parvalbumins
Rats, Wistar
Nerve Net
Receptors, GABA-A
Evoked Potentials
GABA Antagonists
Excitatory Amino Acid Antagonists
Receptors, N-Methyl-D-Aspartate
Neuronal Plasticity
Membrane Potentials
Inhibitory Postsynaptic Potentials
2-Amino-5-phosphonovalerate
Cerebral Cortex
6-Cyano-7-nitroquinoxaline-2,3-dione
Bicuculline
Long-Term Potentiation
Prefrontal Cortex
Dentate Gyrus
Somatosensory Cortex
Dendritic Spines
Electric Fish
Organ Culture Techniques
Glutamic Acid
Receptors, AMPA
GABA-A Receptor Antagonists
Rats, Long-Evans
Kainic Acid
Epilepsy
Afferent Pathways
Presynaptic Terminals
Picrotoxin
Receptors, Metabotropic Glutamate
Perforant Pathway
N-Methylaspartate
Papio ursinus
Receptors, GABA-B
Tetrodotoxin
S100 Calcium Binding Protein G
Receptors, Kainic Acid
Periodicity
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
Calbindins
Visual Cortex
Calcium
Baclofen
Gerbillinae
Status Epilepticus
Biological Clocks
GABA Agonists
Entorhinal Cortex
Differential Threshold
Calbindin 2
Seizures
Olfactory Pathways
4-Aminopyridine
Receptors, Presynaptic
Pilocarpine
Phosphinic Acids
Immunohistochemistry
Long-Term Synaptic Depression
Macaca fascicularis
Glutamate Decarboxylase
GABA Agents
Guinea Pigs
GABA-B Receptor Antagonists
Receptors, Glutamate
Cell Count
Potassium Channels
Tetany
Neural Conduction
Neurotransmitter Agents
Kindling, Neurologic
Convulsants
Receptors, GABA
Maze Learning
Rats, Inbred Strains
Cholecystokinin
Carbachol
Memory
Receptor, Cannabinoid, CB1
Microscopy, Immunoelectron
Electroencephalography
Dose-Response Relationship, Radiation
Epilepsy, Temporal Lobe
Potassium
Isoquinolines
Motor Cortex
Muscarinic Agonists
Glutamates
Computer Simulation
Cycloleucine
Mice, Knockout
GABA Modulators
Feedback
Vibrissae
Mice, Transgenic
Miniature Postsynaptic Potentials
Cholinergic Agents
Dizocilpine Maleate
Microelectrodes
Cannabinoid Receptor Antagonists
Cats
Extracellular Space
Brain
Calcium Channels, P-Type
Electrodes, Implanted
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
Optogenetics
Silver Staining
Sodium Channels
alpha-Mannosidosis
Ibotenic Acid
Calcium Channel Blockers
Analysis of Variance
Receptors, Neurotransmitter
Isonicotinic Acids
Glycine
Cochlear Nucleus
Sodium Channel Blockers
GABA Plasma Membrane Transport Proteins
Calbindin 1
Electrophysiological Phenomena
Spatial Behavior
Neural Networks (Computer)
Methoxyhydroxyphenylglycol
Riluzole
Receptors, Serotonin
Cannabinoid Receptor Modulators
Aging
Calcium Channels
Diazepam
Potassium Channel Blockers
Lateral Line System
Receptor, Metabotropic Glutamate 5
Auditory Cortex
CA2 Region, Hippocampal
Ion Channel Gating
Iontophoresis
Receptors, Dopamine D1
Chelating Agents
Somatostatin
Biotin
Carisoprodol
Endocannabinoids
Microscopy, Electron
Hypoxia, Brain
Nerve Fibers
Nerve Endings
Macaca mulatta
Developmental synaptic changes increase the range of integrative capabilities of an identified excitatory neocortical connection. (1/3377)
Excitatory synaptic transmission between pyramidal cells and fast-spiking (FS) interneurons of layer V of the motor cortex was investigated in acute slices by using paired recordings at 30 degrees C combined with morphological analysis. The presynaptic and postsynaptic properties at these identified central synapses were compared between 3- and 5-week-old rats. At these two postnatal developmental stages, unitary EPSCs were mediated by the activation of AMPA receptors with fast kinetics at a holding potential of -72 mV. The amplitude distribution analysis of the EPSCs indicates that, at both stages, pyramidal-FS connections consisted of multiple functional release sites. The apparent quantal size obtained by decreasing the external calcium ([Ca2+]e) varied from 11 to 29 pA near resting membrane potential. In young rats, pairs of presynaptic action potentials elicited unitary synaptic responses that displayed paired-pulse depression at all tested frequencies. In older animals, inputs from different pyramidal cells onto the same FS interneuron had different paired-pulse response characteristics and, at most of these connections, a switch from depression to facilitation occurred when decreasing the rate of presynaptic stimulation. The balance between facilitation and depression endows pyramidal-FS connections from 5-week-old animals with wide integrative capabilities and confers unique functional properties to each synapse. (+info)Metrifonate increases neuronal excitability in CA1 pyramidal neurons from both young and aging rabbit hippocampus. (2/3377)
The effects of metrifonate, a second generation cholinesterase inhibitor, were examined on CA1 pyramidal neurons from hippocampal slices of young and aging rabbits using current-clamp, intracellular recording techniques. Bath perfusion of metrifonate (10-200 microM) dose-dependently decreased both postburst afterhyperpolarization (AHP) and spike frequency adaptation (accommodation) in neurons from young and aging rabbits (AHP: p < 0.002, young; p < 0.050, aging; accommodation: p < 0.024, young; p < 0.001, aging). These reductions were mediated by muscarinic cholinergic transmission, because they were blocked by addition of atropine (1 microM) to the perfusate. The effects of chronic metrifonate treatment (12 mg/kg for 3 weeks) on CA1 neurons of aging rabbits were also examined ex vivo. Neurons from aging rabbits chronically treated with metrifonate had significantly reduced spike frequency accommodation, compared with vehicle-treated rabbits. Chronic metrifonate treatment did not result in a desensitization to metrifonate ex vivo, because bath perfusion of metrifonate (50 microM) significantly decreased the AHP and accommodation in neurons from both chronically metrifonate- and vehicle-treated aging rabbits. We propose that the facilitating effect of chronic metrifonate treatment on acquisition of hippocampus-dependent tasks such as trace eyeblink conditioning by aging subjects may be caused by this increased excitability of CA1 pyramidal neurons. (+info)Effect of riluzole on the neurological and neuropathological changes in an animal model of cardiac arrest-induced movement disorder. (3/3377)
Posthypoxic myoclonus and seizures precipitate as secondary neurological consequences in ischemic/hypoxic insults of the central nervous system. Neuronal hyperexcitation may be due to excessive activation of glutamatergic neurotransmission, an effect that has been shown to follow ischemic/hypoxic events. Therefore, riluzole, an anticonvulsant that inhibits the release of glutamate by stabilizing the inactivated state of activated voltage-sensitive sodium channels, was tested for its antimyoclonic and neuroprotective properties in the cardiac arrest-induced animal model of posthypoxic myoclonus. Riluzole (4-12 mg/kg i.p.) dose-dependently attenuated the audiogenic seizures and action myoclonus seen in this animal model. Histological examination using Nissl staining and the novel Fluoro-Jade histochemistry in cardiac-arrested animals showed an extensive neuronal degeneration in the hippocampus and cerebellum. Riluzole treatment almost completely prevented the neuronal degeneration in these brain areas. The neuroprotective effect was more pronounced in hippocampal pyramidal neurons and cerebellar Purkinje cells. These effects were seen at therapeutically relevant doses of riluzole, and the animals tolerated the treatment well. These findings indicate that the pathogenesis of posthypoxic myoclonus and seizure may involve excessive activation of glutamate neurotransmission, and that riluzole may serve as an effective pharmacological agent with neuroprotective potential for the treatment of neurological conditions associated with cardiac arrest in humans. (+info)Bilirubin, formed by activation of heme oxygenase-2, protects neurons against oxidative stress injury. (4/3377)
Heme oxygenase (HO) catalyzes the conversion of heme to carbon monoxide, iron, and biliverdin, which is immediately reduced to bilirubin (BR). Two HO active isozymes exist: HO1, an inducible heat shock protein, and HO2, which is constitutive and highly concentrated in neurons. We demonstrate a neuroprotective role for BR formed from HO2. Neurotoxicity elicited by hydrogen peroxide in hippocampal and cortical neuronal cultures is prevented by the phorbol ester, phorbol 12-myristate 13-acetate (PMA) via stimulation of protein kinase C. We observe phosphorylation of HO2 through the protein kinase C pathway with enhancement of HO2 catalytic activity and accumulation of BR in neuronal cultures. The neuroprotective effects of PMA are prevented by the HO inhibitor tin protoporphyrin IX and in cultures from mice with deletion of HO2 gene. Moreover, BR, an antioxidant, is neuroprotective at nanomolar concentrations. (+info)Long-term suppression of synaptic transmission by tetanization of a single pyramidal cell in the mouse hippocampus in vitro. (5/3377)
1. The consequences of stimulating a single pyramidal cell in the CA1 area of the hippocampus for synaptic transmission in the stratum radiatum were investigated. 2. Tetanic activation of single pyramids caused by depolarizing current injection, but not an equal number of distributed action potentials, reduced excitatory transmission by 20 %, with a delayed onset, for more than 1 h. 3. EPSPs in the tetanized pyramidal cells were increased for equally long periods but this was not the cause of the field EPSP reduction. Spontaneous somatic IPSPs were not affected; evoked IPSPs were decreased in the tetanized cell. 4. Paired pulse facilitation of the field EPSPs was unchanged. 5. The field EPSP reduction was markedly diminished by a knife cut along the base of pyramidal cells in CA1. 6. The addition of antagonists of GABA, NMDA and metabotropic glutamate receptors blocked or diminished the field EPSP slope reduction evoked by intracellular stimulation. 7. Simultaneous recordings revealed long-lasting excitations of interneurons located in the outer oriens layer as a result of single pyramid tetanization. 8. Intense firing of small numbers of pyramidal cells can thus persistently inhibit mass transmission through the hippocampus. This effect involves activation of interneurons by glutamate receptors. (+info)Synaptic transmission at nicotinic acetylcholine receptors in rat hippocampal organotypic cultures and slices. (6/3377)
1. Whole-cell clamp recordings of the compound synaptic current elicited by afferent stimulation of Schaffer collaterals showed that blockade of the NMDA, AMPA and GABAA receptor-mediated components by 6-nitro-7-sulphamoyl- benzo(f)quinoxaline-2,3-dione (NBQX), 3-((R)-2-carboxypiperazine-4-yl)propyl-1-phosphonate (R-CPP) and picrotoxin, respectively, left a small residual current in 39 out of 41 CA1 pyramidal neurones in organotypic cultures and 9 out of 16 CA1 cells in acutely prepared slices. 2. This current represented 2. 9 +/- 0.4 % of the compound evoked synaptic response in organoypic cultures and 1.4 +/- 0.5 % in slices. It was characterized by a slightly rectifying I-V curve and a reversal potential of 3.4 +/- 5. 1 mV. 3. This residual current was insensitive to blockers of GABAB, purinergic, muscarinic and 5-HT3 receptors, but it was essentially blocked by the nicotinic receptor antagonist d-tubocurarine (91 +/- 4 % blockade; 20 microM), and partly blocked by alpha-bungarotoxin (200 nM) and methyllycaconitine (10 nM), two antagonists with a higher selectivity for alpha7 subunit-containing nicotinic receptors (48 +/- 3 % and 55 +/- 11 % blockade, respectively). 4. The residual current was of synaptic origin, since it occurred after a small delay; its amplitude depended upon the stimulation intensity and it was calcium dependent and blocked by the sodium channel antagonist tetrodotoxin. 5. We conclude that afferent stimulation applied in the stratum radiatum evokes in some hippocampal neurones a small synaptic current mediated by activation of neuronal nicotinic receptors. (+info)Linear summation of excitatory inputs by CA1 pyramidal neurons. (7/3377)
A fundamental problem in neurobiology is understanding the arithmetic that dendrites use to integrate inputs. The impact of dendritic morphology and active conductances on input summation is still unknown. To study this, we use glutamate iontophoresis and synaptic stimulation to position pairs of excitatory inputs throughout the apical, oblique, and basal dendrites of CA1 pyramidal neurons in rat hippocampal slices. Under a variety of stimulation regimes, we find a linear summation of most input combinations that is implemented by a surprising balance of boosting and shunting mechanisms. Active conductances in dendrites paradoxically serve to make summation linear. This "active linearity" can reconcile predictions from cable theory with the observed linear summation in vivo and suggests that a simple arithmetic is used by apparently complex dendritic trees. (+info)Carbamazepine facilitates effects of GABA on rat hippocampus slices. (8/3377)
AIM: To study the influence of carbamazepine (Car) on GABA effect in hippocampus. METHODS: Evoked potentials were recorded on pyramidal cells in CA1 after stimulation (0.5 Hz, 50 microseconds) to Schaffer collaterals in rat hippocampal slices (350 microns). RESULTS: Car 0.1 and 0.2 mmol.L-1 did not affect field potentials, whereas Car 0.2 mmol.L-1 plus GABA (0.1-1 mmol.L-1) gave rise to a stronger inhibition on field potentials than that of GABA alone. Bicuculline did not reverse Car facilitation on GABA inhibition on field potentials. (-)-Baclofen was more effective in inhibiting field potentials than GABA. Car 0.2 mmol.L-1 plus (-)-baclofen (1-5 mumol.L-1) brought an inhibition stronger than that of (-)-baclofen alone. CONCLUSION: Car facilitates the effects of GABA on pyramidal cells in hippocampal CA1 region, probably related to GABAB receptors. (+info)There are many different types of epilepsy, each with its own unique set of symptoms and characteristics. Some common forms of epilepsy include:
1. Generalized Epilepsy: This type of epilepsy affects both sides of the brain and can cause a range of seizure types, including absence seizures, tonic-clonic seizures, and atypical absence seizures.
2. Focal Epilepsy: This type of epilepsy affects only one part of the brain and can cause seizures that are localized to that area. There are several subtypes of focal epilepsy, including partial seizures with complex symptoms and simple partial seizures.
3. Tonic-Clonic Epilepsy: This type of epilepsy is also known as grand mal seizures and can cause a loss of consciousness, convulsions, and muscle stiffness.
4. Lennox-Gastaut Syndrome: This is a rare and severe form of epilepsy that typically develops in early childhood and can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.
5. Dravet Syndrome: This is a rare genetic form of epilepsy that typically develops in infancy and can cause severe, frequent seizures.
6. Rubinstein-Taybi Syndrome: This is a rare genetic disorder that can cause intellectual disability, developmental delays, and various types of seizures.
7. Other forms of epilepsy include Absence Epilepsy, Myoclonic Epilepsy, and Atonic Epilepsy.
The symptoms of epilepsy can vary widely depending on the type of seizure disorder and the individual affected. Some common symptoms of epilepsy include:
1. Seizures: This is the most obvious symptom of epilepsy and can range from mild to severe.
2. Loss of consciousness: Some people with epilepsy may experience a loss of consciousness during a seizure, while others may remain aware of their surroundings.
3. Confusion and disorientation: After a seizure, some people with epilepsy may feel confused and disoriented.
4. Memory loss: Seizures can cause short-term or long-term memory loss.
5. Fatigue: Epilepsy can cause extreme fatigue, both during and after a seizure.
6. Emotional changes: Some people with epilepsy may experience emotional changes, such as anxiety, depression, or mood swings.
7. Cognitive changes: Epilepsy can affect cognitive function, including attention, memory, and learning.
8. Sleep disturbances: Some people with epilepsy may experience sleep disturbances, such as insomnia or sleepiness.
9. Physical symptoms: Depending on the type of seizure, people with epilepsy may experience physical symptoms such as muscle weakness, numbness or tingling, and sensory changes.
10. Social isolation: Epilepsy can cause social isolation due to fear of having a seizure in public or stigma associated with the condition.
It's important to note that not everyone with epilepsy will experience all of these symptoms, and some people may have different symptoms depending on the type of seizure they experience. Additionally, some people with epilepsy may experience additional symptoms not listed here.
There are two main types of status epilepticus:
1. Generalized status epilepticus: This type affects the entire brain and is characterized by severe convulsions, loss of consciousness, and muscle stiffness.
2. Focal status epilepticus: This type affects only one part of the brain and can cause more subtle symptoms, such as weakness or numbness in a limb, speech difficulties, or confusion.
The diagnosis of status epilepticus is based on clinical findings, medical history, and electroencephalography (EEG) recordings. Treatment typically involves prompt administration of anticonvulsant medications, such as benzodiazepines or barbiturates, to control seizures and prevent further brain damage. In severe cases, sedation, mechanical ventilation, or anesthesia may be required to support the patient's vital functions.
The prognosis for status epilepticus depends on several factors, including the underlying cause, the severity of the seizure, and the promptness and effectiveness of treatment. In general, the earlier the treatment is initiated, the better the outcome. However, long-term neurological and cognitive deficits can occur in some cases.
Preventive measures for status epilepticus include proper management of underlying conditions that may trigger seizures, such as epilepsy or head trauma, and avoiding triggers like alcohol or drugs. Additionally, prompt medical attention should be sought if seizure warning signs are present, such as changes in sensation, confusion, or convulsions.
There are many different types of seizures, each with its own unique set of symptoms. Some common types of seizures include:
1. Generalized seizures: These seizures affect both sides of the brain and can cause a range of symptoms, including convulsions, loss of consciousness, and muscle stiffness.
2. Focal seizures: These seizures affect only one part of the brain and can cause more specific symptoms, such as weakness or numbness in a limb, or changes in sensation or vision.
3. Tonic-clonic seizures: These seizures are also known as grand mal seizures and can cause convulsions, loss of consciousness, and muscle stiffness.
4. Absence seizures: These seizures are also known as petit mal seizures and can cause a brief loss of consciousness or staring spell.
5. Myoclonic seizures: These seizures can cause sudden, brief muscle jerks or twitches.
6. Atonic seizures: These seizures can cause a sudden loss of muscle tone, which can lead to falls or drops.
7. Lennox-Gastaut syndrome: This is a rare and severe form of epilepsy that can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.
Seizures can be diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electroencephalography (EEG) or imaging studies. Treatment for seizures usually involves anticonvulsant medications, but in some cases, surgery or other interventions may be necessary.
Overall, seizures are a complex and multifaceted symptom that can have a significant impact on an individual's quality of life. It is important to seek medical attention if you or someone you know is experiencing seizures, as early diagnosis and treatment can help to improve outcomes and reduce the risk of complications.
Epilepsy, temporal lobe can cause a variety of seizure types, including:
1. Partial seizures: These are seizures that affect only one part of the brain, such as the temporal lobe.
2. Simple partial seizures: These are seizures that do not involve convulsions or loss of consciousness.
3. Complex partial seizures: These are seizures that involve impaired awareness or altered perception, and may involve convulsions or muscle stiffness.
4. Tonic-clonic seizures (formerly known as grand mal seizures): These are seizures that involve convulsions, loss of consciousness, and muscle stiffness.
The symptoms of epilepsy, temporal lobe can vary depending on the location of the seizure focus within the temporal lobe and the individual's age, but may include:
1. Auras (sensory disturbances such as flashing lights or unusual smells)
2. Confusion or disorientation
3. Memory loss or difficulty with memory
4. Emotional changes (such as fear, anxiety, or euphoria)
5. Speech difficulties
6. Muscle stiffness or weakness
7. Coordination problems
8. Vision changes (such as blurred vision or double vision)
9. Hearing changes (such as ringing in the ears)
10. Numbness or tingling sensations
Epilepsy, temporal lobe is typically diagnosed using a combination of medical history, physical examination, and diagnostic tests such as electroencephalography (EEG) or magnetic resonance imaging (MRI). Treatment options may include medication, surgery, or lifestyle modifications.
The symptoms of alpha-mannosidosis typically appear during childhood and can include:
* Developmental delays and intellectual disability
* Coarse facial features, such as a prominent forehead, large ears, and widely spaced eyes
* Poor muscle tone and motor skills
* Vision loss or blindness
* Hearing loss or deafness
* Respiratory problems
* Cardiac problems
* Increased risk of infections
If left untreated, alpha-mannosidosis can lead to a range of complications, including:
* Progressive intellectual disability
* Seizures
* Poor coordination and balance
* Increased risk of infections and respiratory problems
* Malformation of the brain and other organs
There is currently no cure for alpha-mannosidosis, but treatment options are available to manage the symptoms and slow the progression of the disease. These may include:
* Enzyme replacement therapy: This involves replacing the missing enzyme with a synthetic version to help break down the sugars that build up in the body.
* Vitamin supplements: Certain vitamins, such as vitamin E, may be prescribed to help manage some of the symptoms of alpha-mannosidosis.
* Physical therapy: This can help improve muscle tone and coordination.
* Occupational therapy: This can help individuals with alpha-mannosidosis learn new skills and adapt to their condition.
* Speech therapy: This can help improve communication and address any hearing or speech difficulties.
Early diagnosis and treatment of alpha-mannosidosis are crucial to managing the symptoms and slowing the progression of the disease. If you suspect that your child may have alpha-mannosidosis, it is important to speak with a healthcare professional as soon as possible. They can perform tests to confirm the diagnosis and recommend appropriate treatment options. With early diagnosis and proper management, individuals with alpha-mannosidosis can lead fulfilling lives and achieve their full potential.
Brain hypoxia is a serious medical condition that requires prompt treatment to prevent long-term damage and improve outcomes for patients. Treatment options may include oxygen therapy, medications to improve blood flow to the brain, and surgery to remove any blockages or obstructions in blood vessels.
Pyramidal cell
Pyramidal tracts
Gene therapy for epilepsy
KCNK9
Hippocampus anatomy
Temporal lobe epilepsy
Hirano body
Neurotoxin
Oscar Marín
Inhibitory postsynaptic potential
SPOCK1
Upper motor neuron
Critical period
Wynnea americana
Oskar Vogt
Feature detection (nervous system)
Martinotti cell
Brodmann area 20
Isothalamus
Neuronal tracing
Glucocorticoids in hippocampal development
Neural backpropagation
Large irregular activity
Optogenetics
Brodmann area 14
HCN1
Fear conditioning
Panayiota Poirazi
Phase precession
Brodmann area 4
Racemization
Afterhyperpolarization
Rotational-vibrational spectroscopy
Congenital mirror movement disorder
Lepiota nirupama
Hexagonal crystal family
Metabotropic glutamate receptor
Ammonia
Sutton Hoo
Trichoderma
Hippocampal memory encoding and retrieval
Brain
Colton Point State Park
Tetradentate ligand
Iridium
Intermediate progenitor cell
Close-packing of equal spheres
Connectome
Code Saturne
St Patrick's Convent, North Ward
Corticospinal tract
Toowoomba Police Station Complex
Michael Kaplan (biologist)
Synaptic noise
Phosphine
Precentral gyrus
Scratch reflex
Gerstmann-Sträussler-Scheinker syndrome
ICI-118,551
NIMH » Pyramidal cells
Dendritic Na+ channels amplify EPSPs in hippocampal CA1 pyramidal cells - PubMed
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Selective expression of ErbB4 in interneurons, but not pyramidal cells, of the rodent hippocampus - PubMed
ModelDB: Feedforward inhibition in pyramidal cells (Ferrante & Ascoli 2015)
FMRP regulates mRNAs encoding distinct functions in the cell body and dendrites of CA1 pyramidal neurons | eLife
Pyramidal Cells | Profiles RNS
NeuroElectro :: Olfactory cortex pyramidal cell
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Cytochrome-oxidase blobs and intrinsic horizontal connections of layer 2/3 pyramidal neurons in primate V1
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Russell Kightley Scientific Illustrator & Animator | Pyramidal Cell from Brain 1 (Rights Managed)
Pyramidal Cell In Cerebral Cortex, Cajal Beach Towel by Science Source - Science Source Prints - Website
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Slide 6 | McCormick Lab
Rounded Rear Pyramidal Text... - Researchers - ANU
Publication Detail
Santiago Ramón y Cajal Exhibit - Office of NIH History and Stetten Museum
Spine Neck Plasticity Controls Postsynaptic Calcium Signals through Electrical Compartmentalization | Journal of Neuroscience
principal neuron - German missing: English ⇔ German Forums - leo.org
A null model of the mouse whole-neocortex micro-connectome | Nature Communications
NAEC Meeting Minutes - January 11, 2019 | National Eye Institute
Qualia - Wikipedia
Synaptic & Developmental Plasticity Group - Regulation of Synaptic Effectiveness
CDC - Diagnosis: Histologic Examination - Rabies
MESH TREE NUMBER CHANGES - 2008 MeSH
Neurons29
- 1. Whole cell recordings were performed on the somata of CA1 pyramidal neurons in the rat hippocampal slice preparation Remote synaptic events were evoked by electrical stimulation of Schaffer collateral/commissural fibers in outer stratum radiatum. (nih.gov)
- 2019). Homogenates of AD brain samples hence naturally include potential changes originating in glial cells, vascular cells, blood cells, and matrix components in addition to altered numbers and contents of neurons, making bulk analysis difficult to interpret (De Marchi et al. (proquest.com)
- 2019). Hippocampal cornu ammonis 1 (CA1) and CA3 are areas rich in pyramidal neurons, mainly involved in memory formation, and severely affected in AD as reflected in models for AD (Kuczynski et al. (proquest.com)
- We have previously applied LCM to study both intra-neuronal Aβ in isolated hippocampal neurons from post-mortem AD brain and the combined proteome of isolated hippocampal pyramidal neurons pooled from six AD and six neurologically healthy cases, respectively (Aoki et al. (proquest.com)
- We detected ErbB4 immunoreactivity in GABAergic interneurons but not in pyramidal neurons, a finding that was further corroborated by the lack of ErbB4 mRNA in electrophysiologically identified pyramidal neurons as determined by single-cell reverse transcription-PCR. (nih.gov)
- Here we develop a strategy combining compartment-specific CLIP and TRAP in conditionally tagged mice to precisely define the ribosome-bound dendritic transcriptome of CA1 pyramidal neurons. (elifesciences.org)
- Pyramidal neurons in superficial layers of cerebral cortex have extensive horizontal axons that provide a substrate for lateral interactions across cortical columns. (nih.gov)
- To better understand the precise relationship between horizontal connections and blobs, we intracellularly labeled 20 layer 2/3 pyramidal neurons in tangential living brain slices from V1 of macaque monkeys. (nih.gov)
- The distant synaptic boutons from these cells were generally located relatively near to blob centers, but the neurons closest to blob centers had synaptic boutons closer to blob centers than those farther away. (nih.gov)
- Pyramidal cells (neurons) are found in the cortex of the brain. (scientific.pictures)
- Pyramidal neurons (pyramidal cells) are a type of. (sciencesource.com)
- Pyramidal neurons (pyramidal cells) are a type of neuron found in areas of the brain including the cerebral cortex, the hippocampus, and the amygdala. (sciencesource.com)
- Pyramidal neurons are the primary excitation units of the mammalian prefrontal cortex and the corticospinal tract. (sciencesource.com)
- Pyramidal neurons were first discovered and studied by Santiago Ramon y Cajal. (sciencesource.com)
- Since then, studies on pyramidal neurons have focused on topics ranging from neuroplasticity to cognition. (sciencesource.com)
- This response was primarily observed in pyramidal neurons with little non-neuronal expression. (nih.gov)
- Mouse hippocampal neurons labeled with green or red fluorescent proteins can be used to study specific populations of pyramidal cells. (nih.gov)
- Here neurons in area CA2 appear green and CA3 pyramidal cells and dentate gyrus granule cells red. (nih.gov)
- Neuronal necrosis should be carefully differentiated from dark neuron artifact (see Brain - Introduction ) by screening for various stages of necrosis and/or the presence of inflammatory cells or other lesions in the vicinity of the truly necrotic neurons. (nih.gov)
- In this case, the appearance of these necrotic neurons can be contrasted with the more normal morphology of an adjacent Purkinje cell (red arrow). (nih.gov)
- Fluorescence of affected cells highlights the injured neurons, but the use of hematoxylin and eosin is also important to identify associated neural changes corroborating the fluorescent findings and defining the chronology of the lesions. (nih.gov)
- Fluoro-Jade C is the most recent of the Fluoro-Jade stains and has been found to stain all degenerating neurons, regardless of specific insult or mechanism of cell death. (nih.gov)
- Activated astrocytes, degenerating neurons, and cell nuclei can be labeled together using glial fibrillary acidic protein immunofluorescence, Fluoro-Jade C, and 4'',6-diamidino-2-phenylindole (DAPI), respectively. (nih.gov)
- The presence of more normal neurons in adjacent areas assists with the recognition of these forms of degenerate cells differentiating the changes from that of autolysis. (nih.gov)
- D) Cerebellum showing severe depletion of Purkinje neurons and acute neuronal death (arrows and inset [original magnification ×40]) with relative sparing of the internal granule cell layer (arrowheads) and inflammation (short arrows) (original magnification ×10). (cdc.gov)
- It is rich in pyramidal neurons, which provide the anatomical substrates for the motor output function of area 4. (medscape.com)
- Dendritic spines, tiny "thorns," or projections from the dendrites of a nerve cell, serve as receivers in many of the synaptic contacts between neurons. (scientificamerican.com)
- Their analysis focused on deep-layer pyramidal prelimbic cortex neurons because these cells reach into areas of the brain that have been implicated in drug-seeking behaviors. (nih.gov)
- The scientists employed a light-based genetic, or optogenetic, technique to activate or inhibit pyramidal neurons in the prelimbic cortex at will. (nih.gov)
Hippocampus3
- Feedforward inhibition (FFI) enables pyramidal cells in area CA1 of the hippocampus (CA1PCs) to remain easily excitable while faithfully representing a broad range of excitatory inputs without quickly saturating. (yale.edu)
- We previously reported that ABA in adolescent female rats results in increased apical dendritic branching in CA1 pyramidal cells of the ventral hippocampus at postnatal day 44 (P44). (nyu.edu)
- C) Pyramidal cell layer of the hippocampus showing extensive acute neuronal death (arrows) (original magnification ×4). (cdc.gov)
Neuron5
- Emerging from the base of the neuron is a slender axon, which transmits nerve impulses away from the cell body. (scientific.pictures)
- The principal neuron in the cerebellum is the Purkinje cell. (leo.org)
- The principal neuron in the cerebellar cortex is the Purkinje cell. (leo.org)
- Promoting regeneration while blocking cell death preserves motor neuron function in a model of ALS. (nih.gov)
- The drawing is of a type of cortical neuron known as the pyramidal cell. (scientificamerican.com)
Cortical4
- These results reveal a remarkable association between arousal level and membrane potential of some cortical pyramidal cells. (yale.edu)
- Parabolic avalanche scaling in the synchronization of cortical cell assemblies. (nih.gov)
- We then discuss how the involvement of multiple cell types, each with a specific set of cellular properties, plays a crucial role in diversifying and increasing the computational power of a relatively small number of simple circuit motifs forming cortical networks. (nih.gov)
- A) Cortical neuronal somata reconstruction to aid in cortical layer boundaries (dotted lines) based on cell number and size. (scienceblogs.com)
Synaptic6
- FMRP regulates ~15-20% of mRNAs encoding synaptic functions and 10% of chromatin modulators, in the dendrite and cell body, respectively. (elifesciences.org)
- Together, the data support a model in which FMRP regulates the translation and expression of synaptic and nuclear proteins within different compartments of a single neuronal cell type. (elifesciences.org)
- The locations of each cell body and the cell's synaptic boutons relative to blobs were quantitatively analyzed. (nih.gov)
- For all cells, synaptic boutons close to the cell body were located at similar distances from blob centers as the cell body. (nih.gov)
- Serena M. Dudek, Ph.D., is Deputy Chief of the Neurobiology Laboratory, head of the Synaptic and Developmental Plasticity Group, and holds a secondary appointment in the NIEHS Epigenetics and Stem Cell Biology Laboratory . (nih.gov)
- Synaptic junctions between nerve cells can be between axon and dendritic spine or between axon and the dendrite itself. (scientificamerican.com)
Cerebral cortex1
- There are no comments for Pyramidal Cell In Cerebral Cortex, Cajal . (sciencesource.com)
Synapses2
- It was impressive that they managed to get a complete record of 1500 µm 3 of the brain, with a complete map of all the cells and synapses. (scienceblogs.com)
- Studies show that a reduction of SynGAP activity can have multiple effects in nerve cells, including pushing synapses to develop too early. (medlineplus.gov)
Rats6
- New findings about comparing the effects of antibiotic therapy and phage therapy on memory and hippocampal pyramidal cells in rats. (bvsalud.org)
- Rats from an enriched environment have more spines on these cells than their littermates from an impoverished environment. (scientificamerican.com)
- The researchers compared nerve cell firing patterns in the brains of the shock-sensitive and shock-resistant groups of rats. (nih.gov)
- Tiny optic fibers were implanted in the rats' brains to deliver light pulses to the cells. (nih.gov)
- As predicted, activating these brain cells reduced cocaine seeking in the compulsive, shock-resistant rats. (nih.gov)
- Inhibiting the cells in shock-sensitive rats increased cocaine seeking during foot-shock sessions. (nih.gov)
Somata1
- These two layer VI pyramidal cell somata (red and green arrows) give rise to the apical dendrites that form the core of the saturated cylinders. (scienceblogs.com)
Interneurons3
- FFI in CA1PCs is mediated by two physiologically and morphologically distinct GABAergic interneurons: fast-spiking, perisomatic-targeting basket cells and regular-spiking, dendritic-targeting bistratified cells. (yale.edu)
- 1 . Ferrante M, Ascoli GA (2015) Distinct and synergistic feedforward inhibition of pyramidal cells by basket and bistratified interneurons. (yale.edu)
- Extrinsic and local glutamatergic inputs of the rat hippocampal CA1 area differentially innervate pyramidal cells and interneurons. (ox.ac.uk)
Granule1
- Intrahippocampal N-MDA also increased hippocampal CHAT activity and resulted in a loss of pyramidal and dentate granule cells. (nih.gov)
Hippocampal slice1
- A metabolically stable analog of 1,4,5-inositol trisphosphate activates a novel K+ conductance in pyramidal cells of the rat hippocampal slice. (ox.ac.uk)
Corticospinal tract1
- In humans, only 5% of the fibers of the corticospinal tract originate from Betz cells in area 4. (medscape.com)
Axon7
- 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. (uams.edu)
- The majority of boutons from cells lacking distal axon clusters were close to their cell bodies. (nih.gov)
- Cells located more than 200 microm from blob centers were in interblobs and had long-distance clustered axon collaterals selectively targeting distant interblob regions. (nih.gov)
- The dendrites of pyramidal cells are covered by small projections (dendritic spines) which are the contact point for axon terminals from other nerve cells. (scientific.pictures)
- the dendritic arbor, the cell body, and the axon. (nih.gov)
- DLK-dependent mitochondrial fission drives axon degeneration and neuronal cell death. (nih.gov)
- Properties of action potential initiation in neocortical pyramidal cells: evidence from whole cell axon recordings. (yale.edu)
Differentially1
- Cell-type specific FMRP-CLIP and TRAP in microdissected CA1 neuropil revealed 383 dendritic FMRP targets and suggests that FMRP differentially regulates functionally distinct modules in CA1 dendrites and cell bodies. (elifesciences.org)
Neocortical1
- Here we review our current understanding of neocortical interneuron diversity and the properties that distinguish cell types. (nih.gov)
Dendrites3
- They have an approximately conical cell body with a major dendrite trunk emerging from the top (the apical dendrite) and several dendrites emerging from around the base (the basal dendrites). (scientific.pictures)
- A greenish glow represents a signal travelling towards the cell body along several of these dendrites (especially obvious in the apical dendrite trunk). (scientific.pictures)
- D) The two pyramidal cells (red and green arrows) whose apical dendrites lie in the centers of the saturated reconstructions. (scienceblogs.com)
Glial cells1
- Further, important substantiating evidence of brain tissue injury is represented by the edematous vacuolar change of the subjacent neuropil and the presence of necrotic condensed (pyknotic) nuclei of glial cells (arrowhead) within that region. (nih.gov)
Pathways1
- The concept of pyramidal pathways with fibers originating only from Betz cells in the primary motor cortex has been invalidated. (medscape.com)
Biol1
- J Cell Biol. (nih.gov)
Purkinje1
- They are found most frequently in the pyramidal cells of Ammon's horn, and the Purkinje cells of the cerebellum. (cdc.gov)
Brain6
- Although AD is largely regarded as a gray matter disease, different types of brain cells are affected and are further accompanied by extracellular changes (Mathys et al. (proquest.com)
- Sympathetic ganglia comprises the thousands of afferent and efferent nerve cell bodies that run along either side of the spinal cord, connecting major organ systems, such as the renal system, to the spinal cord and brain. (nih.gov)
- Perivascular inflammatory cell infiltrates in hematoxylin & eosin stained brain tissue. (cdc.gov)
- This panel of brain necrosis images is intended to familiarize pathologists with the morphologic variations of neuronal cell death ranging from the morphology of acute necrosis to that of late stages of necrosis in which mineralization sometimes is prominent. (nih.gov)
- Every once in a while, I get some glib story from believers in the Singularity and transhumanism that all we have to do to upload a brain into a computer is make lots of really thin sections and reconstruct every single cell and every single connection, put that data into a machine with a sufficiently robust simulator that executes all the things that a living brain does, and presto! (scienceblogs.com)
- The protein produced from this gene, called SynGAP, plays an important role in nerve cells in the brain. (medlineplus.gov)
ErbB41
- However, despite much attention this pathway and its effects on pyramidal cells have received recently, the presence of ErbB4 in these cells is still controversial. (nih.gov)
Layer1
- Whole cell recording from a layer 5 pyramidal cell in the auditory cortex reveals that the membrane potential of these cells closely follows the state of the mouse, as revealed by pupil diameter. (yale.edu)
Activate1
- Thus, IP(s)3 may activate a novel K+ conductance in CA1 pyramidal cells. (ox.ac.uk)
10.10161
- doi: 10.1016/j.cell.2012.08.045. (medlineplus.gov)
Bodies2
- Conversely, downregulation of FMRP targets involved in chromatin regulation in cell bodies and suggest a role for FMRP in stabilizing mRNAs containing stalled ribosomes in this compartment. (elifesciences.org)
- In his report, he described Negri bodies as round or oval inclusions within the cytoplasm of nerve cells of animals infected with rabies. (cdc.gov)
Type1
- Absence of TRIC-B from type XIV Osteogenesis Imperfecta osteoblasts alters cell adhesion and mitochondrial function - A multi-omics study. (nih.gov)
Specific1
- They injected harmless viruses engineered to deliver genes for producing proteins that, once embedded in the neuron's surface, could induce or inhibit the cells' activity in response to light of specific wavelengths. (nih.gov)
Area2
- Dr. Miller has done noteworthy work in the area of regenerative medicine to transplant retinal pigment epithelium (RPE) cells derived from induced pluripotent stem cell (iPSC) fibroblasts into the subretinal space of clinical subjects. (nih.gov)
- only a small portion (3-5%) are large-diameter fibers (10-22mm) that originate in Betz cells from area 4. (medscape.com)
Analyze1
- Paired with the companion software, Neurolucida Explorer , you can quickly and effectively analyze the morphology of subcellular structures, whole cells, or complex connective networks - from any species. (mbfbioscience.com)
Magnification1
- Blood vessel without inflamatory cells (200x magnification). (cdc.gov)
Found4
- Cells located less than 130 microm from blob centers were found within both blobs and interblobs, but many were close to traditionally defined borders. (nih.gov)
- We found that while ABA at P44 resulted in increased branching of ventral hippocampal pyramidal cells, relapse of ABA at P55 resulted in decreased branching. (nyu.edu)
- Cells from control animals were found to exhibit a dramatic increase in branching, more than doubling from P44 to P51, followed by pruning from P51 to P55. (nyu.edu)
- They are also found in the cells of the medulla and various other ganglia. (cdc.gov)
Study1
- [ 2 ] From 1950-1970, several other studies of electrical stimulation of the exposed motor cortex (ie, during neurosurgical procedures) were performed in animals and humans to study the pyramidal pathway and other corticospinal connections. (medscape.com)
Solar1
- TFQD - Thin film light-trapping enhanced quantum dot photovoltaic cells: an enabling technology for high power-to-weight ratio space solar arrays. (polito.it)
Adult1
- The astroglial and stem cell functions of adult rat folliculostellate cells. (nih.gov)