Excitatory Postsynaptic Potentials
Synaptic Transmission
Synapses
Evoked Potentials
Neurons
Hippocampus
2-Amino-5-phosphonovalerate
Neural Inhibition
Pyramidal Cells
Excitatory Amino Acid Antagonists
Action Potentials
Electrophysiology
Patch-Clamp Techniques
Long-Term Potentiation
Receptors, N-Methyl-D-Aspartate
Interneurons
GABA Antagonists
6-Cyano-7-nitroquinoxaline-2,3-dione
Membrane Potentials
Inhibitory Postsynaptic Potentials
Rats, Sprague-Dawley
Glutamic Acid
Dendrites
Presynaptic Terminals
Bicuculline
Receptors, AMPA
Neuronal Plasticity
Picrotoxin
Afferent Pathways
CA1 Region, Hippocampal
Receptors, Presynaptic
N-Methylaspartate
Tetrodotoxin
Cats
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
Rats, Wistar
Receptors, GABA-B
Baclofen
Receptors, Neurotransmitter
Synaptic Membranes
Models, Neurological
GABA-B Receptor Antagonists
Receptors, Glutamate
Ganglia, Invertebrate
Astacoidea
Vestibulocochlear Nerve
Dentate Gyrus
Neurotransmitter Agents
Myenteric Plexus
Spinal Cord
Receptors, GABA-A
Miniature Postsynaptic Potentials
Perforant Pathway
Thalamus
GABA-A Receptor Antagonists
Strychnine
Receptors, Metabotropic Glutamate
Neocortex
Ganglia, Autonomic
Guinea Pigs
Brain Stem
Aplysia
Organ Culture Techniques
Mossy Fibers, Hippocampal
Nerve Fibers
Pyramidal Tracts
Calcium
Microelectrodes
Glutamates
Receptors, Kainic Acid
Submucous Plexus
Ganglia, Parasympathetic
Nerve Net
Glycine
Cerebral Cortex
Cycloleucine
Hermissenda
Decerebrate State
Receptors, GABA
Iontophoresis
GABA Agonists
Oculomotor Nerve
Serotonin
Ganglia, Sympathetic
Somatosensory Cortex
Long-Term Synaptic Depression
Excitatory Amino Acids
Phosphinic Acids
Kainic Acid
Reflex, Monosynaptic
Voltage-Sensitive Dye Imaging
Differential Threshold
Efferent Pathways
Dose-Response Relationship, Radiation
Lampreys
Cerebellum
Dendritic Spines
Electric Fish
Acetylcholine
Spinal Nerve Roots
Hexamethonium
Autonomic Fibers, Preganglionic
Reflex
Geniculate Bodies
Rana catesbeiana
Kindling, Neurologic
Entorhinal Cortex
Rats, Long-Evans
Epilepsy
4-Aminopyridine
Calcium Channel Blockers
Solitary Nucleus
Receptors, Nicotinic
Nicotinic Antagonists
Neural Conduction
Chelating Agents
Drug Interactions
Feedback
Calcium Channels
Mechanoreceptors
Post-Synaptic Density
Dose-Response Relationship, Drug
Glycine Agents
Olfactory Pathways
Rats, Inbred Strains
Olfactory Bulb
Receptors, Serotonin
Cells, Cultured
Excitatory Amino Acid Agents
Vagus Nerve
Dopamine
Valine
Benzothiadiazines
Small-Conductance Calcium-Activated Potassium Channels
Cochlear Nucleus
Potassium Channel Blockers
Naloxone
Magnesium
Substantia Gelatinosa
Potassium Channels
Atropine
Substance P
Corpus Striatum
Locomotion
Reflex, Stretch
Ileum
Carbachol
Mice, Knockout
Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
Synaptic Vesicles
Sodium Channel Blockers
Adenosine
Medulla Oblongata
Sodium Channels
Amygdala
Brain
Muscle Spindles
Posterior Horn Cells
Enkephalin, Methionine
Dizocilpine Maleate
Auditory Pathways
Computer Simulation
Ion Channel Gating
Immunohistochemistry
Periaqueductal Gray
CA3 Region, Hippocampal
Pons
Thalamic Nuclei
Ganglia
Receptors, Amino Acid
Quisqualic Acid
The functional anatomy of the normal human auditory system: responses to 0.5 and 4.0 kHz tones at varied intensities. (1/5056)
Most functional imaging studies of the auditory system have employed complex stimuli. We used positron emission tomography to map neural responses to 0.5 and 4.0 kHz sine-wave tones presented to the right ear at 30, 50, 70 and 90 dB HL and found activation in a complex neural network of elements traditionally associated with the auditory system as well as non-traditional sites such as the posterior cingulate cortex. Cingulate activity was maximal at low stimulus intensities, suggesting that it may function as a gain control center. In the right temporal lobe, the location of the maximal response varied with the intensity, but not with the frequency of the stimuli. In the left temporal lobe, there was evidence for tonotopic organization: a site lateral to the left primary auditory cortex was activated equally by both tones while a second site in primary auditory cortex was more responsive to the higher frequency. Infratentorial activations were contralateral to the stimulated ear and included the lateral cerebellum, the lateral pontine tegmentum, the midbrain and the medial geniculate. Contrary to predictions based on cochlear membrane mechanics, at each intensity, 4.0 kHz stimuli were more potent activators of the brain than the 0.5 kHz stimuli. (+info)Developmental synaptic changes increase the range of integrative capabilities of an identified excitatory neocortical connection. (2/5056)
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)Modulation of long-term synaptic depression in visual cortex by acetylcholine and norepinephrine. (3/5056)
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)Plasticity of first-order sensory synapses: interactions between homosynaptic long-term potentiation and heterosynaptically evoked dopaminergic potentiation. (4/5056)
Persistent potentiations of the chemical and electrotonic components of the eighth nerve (NVIII) EPSP recorded in vivo in the goldfish reticulospinal neuron, the Mauthner cell, can be evoked by afferent tetanization or local dendritic application of an endogenous transmitter, dopamine (3-hydroxytyramine). These modifications are attributable to the activation of distinct intracellular kinase cascades. Although dopamine-evoked potentiation (DEP) is mediated by the cAMP-dependent protein kinase (PKA), tetanization most likely activates a Ca2+-dependent protein kinase via an increased intracellular Ca2+ concentration. We present evidence that the eighth nerve tetanus that induces LTP does not act by triggering dopamine release, because it is evoked in the presence of a broad spectrum of dopamine antagonists. To test for interactions between these pathways, we applied the potentiating paradigms sequentially. When dopamine was applied first, tetanization produced additional potentiation of the mixed synaptic response, but when the sequence was reversed, DEP was occluded, indicating that the synapses potentiated by the two procedures belong to the same or overlapping populations. Experiments were conducted to determine interactions between the underlying regulatory mechanisms and the level of their convergence. Inhibiting PKA does not impede tetanus-induced LTP, and chelating postsynaptic Ca2+ with BAPTA does not block DEP, indicating that the initial steps of the induction processes are independent. Pharmacological and voltage-clamp analyses indicate that the two pathways converge on functional AMPA/kainate receptors for the chemically mediated EPSP and gap junctions for the electrotonic component or at intermediaries common to both pathways. A cellular model incorporating these interactions is proposed on the basis of differential modulation of synaptic responses via receptor-protein phosphorylation. (+info)Activity-dependent metaplasticity of inhibitory and excitatory synaptic transmission in the lamprey spinal cord locomotor network. (5/5056)
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)GABAergic excitatory synapses and electrical coupling sustain prolonged discharges in the prey capture neural network of Clione limacina. (6/5056)
Afterdischarges represent a prominent characteristic of the neural network that controls prey capture reactions in the carnivorous mollusc Clione limacina. Their main functional implication is transformation of a brief sensory input from a prey into a lasting prey capture response. The present study, which focuses on the neuronal mechanisms of afterdischarges, demonstrates that a single pair of interneurons [cerebral A interneuron (Cr-Aint)] is responsible for afterdischarge generation in the network. Cr-Aint neurons are electrically coupled to all other neurons in the network and produce slow excitatory synaptic inputs to them. This excitatory transmission is found to be GABAergic, which is demonstrated by the use of GABA antagonists, uptake inhibitors, and double-labeling experiments showing that Cr-Aint neurons are GABA-immunoreactive. The Cr-Aint neurons organize three different pathways in the prey capture network, which provide positive feedback necessary for sustaining prolonged spike activity. The first pathway includes electrical coupling and slow chemical transmission from the Cr-Aint neurons to all other neurons in the network. The second feedback is based on excitatory reciprocal connections between contralateral interneurons. Recurrent excitation via the contralateral cell can sustain prolonged interneuron firing, which then drives the activity of all other cells in the network. The third positive feedback is represented by prominent afterdepolarizing potentials after individual spikes in the Cr-Aint neurons. Afterdepolarizations apparently represent recurrent GABAergic excitatory inputs. It is suggested here that these afterdepolarizing potentials are produced by GABAergic excitatory autapses. (+info)Comparative effects of methylmercury on parallel-fiber and climbing-fiber responses of rat cerebellar slices. (7/5056)
The environmental neurotoxicant methylmercury (MeHg) causes profound disruption of cerebellar function. Previous studies have shown that acute exposure to MeHg impairs synaptic transmission in both the peripheral and central nervous systems. However, the effects of MeHg on cerebellar synaptic function have never been examined. In the present study, effects of acute exposure to MeHg on synaptic transmission between parallel fibers or climbing fibers and Purkinje cells were compared in 300- to 350-microm cerebellar slices by using extracellular and intracellular microelectrode-recording techniques. Field potentials of parallel-fiber volleys (PFVs) and the associated postsynaptic responses (PSRs) were recorded in the molecular layer by stimulating the parallel fibers in transverse cerebellar slices. The climbing-fiber responses were also recorded in the molecular layer by stimulating white matter in sagittal cerebellar slices. At 20, 100, and 500 microM, MeHg reduced the amplitude of both PFVs and the associated PSRs to complete block, however, it blocked PSRs more rapidly than PFVs. MeHg also decreased the amplitudes of climbing-fiber responses to complete block. For all responses, an initial increase in amplitude preceded MeHg-induced suppression. Intracellular recordings of excitatory postsynaptic potentials of Purkinje cells were compared before and after MeHg. At 100 microM and 20 microM, MeHg blocked the Na+-dependent, fast somatic spikes and Ca++-dependent, slow dendritic spike bursts. MeHg also hyperpolarized and then depolarized Purkinje cell membranes, suppressed current conduction from parallel fibers or climbing fibers to dendrites of Purkinje cells, and blocked synaptically activated local responses. MeHg switched the pattern of repetitive firing of Purkinje cells generated spontaneously or by depolarizing current injection at Purkinje cell soma from predominantly Na+-dependent, fast somatic spikes to predominantly Ca++-dependent, low amplitude, slow dendritic spike bursts. Thus, acute exposure to MeHg causes a complex pattern of effects on cerebellar synaptic transmission, with apparent actions on both neuronal excitability and chemical synaptic transmission. (+info)Receptor mechanisms underlying heterogenic reflexes among the triceps surae muscles of the cat. (8/5056)
The soleus (S), medial gastrocnemius (MG), and lateral gastrocnemius (LG) muscles of the cat are interlinked by rapid spinal reflex pathways. In the decerebrate state, these heterogenic reflexes are either excitatory and length dependent or inhibitory and force dependent. Mechanographic analysis was used to obtain additional evidence that the muscle spindle primary ending and the Golgi tendon organ provide the major contributions to these reflexes, respectively. The tendons of the triceps surae muscles were separated and connected to independent force transducers and servo-controlled torque motors in unanesthetized, decerebrate cats. The muscles were activated as a group using crossed-extension reflexes. Electrical stimulation of the caudal cutaneous sural nerve was used to provide a particularly strong activation of MG and decouple the forces of the triceps surae muscles. During either form of activation, the muscles were stretched either individually or in various combinations to determine the strength and characteristics of autogenic and heterogenic feedback. The corresponding force responses, including both active and passive components, were measured during the changing background tension. During activation of the entire group, the excitatory, heterogenic feedback linking the three muscles was found to be strongest onto LG and weakest onto MG, in agreement with previous results concerning the strengths of heteronymous Ia excitatory postsynaptic potentials among the triceps surae muscles. The inhibition, which is known to affect only the soleus muscle, was dependent on active contractile force and was detected essentially as rapidly as length dependent excitation. The inhibition outlasted the excitation and was blocked by intravenous strychnine. These results indicate that the excitatory and inhibitory effects are dominated by feedback from primary spindle receptors and Golgi tendon organs. The interactions between these two feedback pathways potentially can influence both the mechanical coupling between ankle and knee. (+info)The term "decerebrate" comes from the Latin word "cerebrum," which means brain. In this context, the term refers to a state where the brain is significantly damaged or absent, leading to a loss of consciousness and other cognitive functions.
Some common symptoms of the decerebrate state include:
* Loss of consciousness
* Flaccid paralysis (loss of muscle tone)
* Dilated pupils
* Lack of responsiveness to stimuli
* Poor or absent reflexes
* Inability to speak or communicate
The decerebrate state can be caused by a variety of factors, including:
* Severe head injury
* Stroke or cerebral vasculature disorders
* Brain tumors or cysts
* Infections such as meningitis or encephalitis
* Traumatic brain injury
Treatment for the decerebrate state is typically focused on addressing the underlying cause of the condition. This may involve medications to control seizures, antibiotics for infections, or surgery to relieve pressure on the brain. In some cases, the decerebrate state may be a permanent condition, and individuals may require long-term care and support.
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 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.
Excitatory postsynaptic potential
Excitatory synapse
Synaptic potential
AMPA
Stimulus (physiology)
Succinic semialdehyde dehydrogenase deficiency
Binding neuron
George Aghajanian
Electrotonic potential
LTP induction
Inhibitory postsynaptic potential
Action potential
SYNGAP1
Auditory cortex
Alpha-1 adrenergic receptor
Acetylcholine
Low-threshold spikes
Temporal lobe epilepsy
Kainic acid
Tetanospasmin
Trk receptor
Adenosine reuptake inhibitor
Non-spiking neuron
Neural circuit
Metabotropic glutamate receptor
Cochlear nucleus
Shunting inhibition
N-Methyl-D-aspartic acid
Population spike
Postsynaptic potential
Pre-Bötzinger complex
Synaptic fatigue
Motion perception
GABAA receptor positive allosteric modulator
Risk factors of schizophrenia
Synaptic noise
GABA transporter type 1
Excitatory amino acid transporter 3
Scratch reflex
Brenda Bloodgood
Losigamone
Glutamate-glutamine cycle
Hippocampus
Glycine receptor
Electroencephalography functional magnetic resonance imaging
Neural backpropagation
John Eccles (neurophysiologist)
Chromatolysis
Nonsynaptic plasticity
Adrenergic nerve fibre
Presynaptic inhibition
Cannabinoid
Retrograde signaling
Granule cell
DLG3
Neuroligin
NMDA receptor
Functional Local Input to Layer 5 Pyramidal Neurons in the Rat Visual Cortex
Plus it
pyramidal spine-neck EPSPs - Page 4 - www.neuron.yale.edu
Epilepsy and Seizures: Practice Essentials, Background, Pathophysiology
Frontiers | Dynamic expression of long noncoding RNAs and repeat elements in synaptic plasticity
Sherrington, Charles Scott | Encyclopedia.com
RS 102221 hydrochloride (CAS 187397-18-8): R&D Systems
Academic Institute - Research output
- Houston Methodist Scholars
William H. Calvin and Derek Bickerton, Lingua ex Machina, chapter 7 (MIT Press)
Faculty of Life Sciences - Research Outputs
- University of Bristol
Internal Medicine - Research output - Mayo Clinic
DeCS
Lack of the peroxiredoxin 6 gene causes impaired spatial memory and abnormal synaptic plasticity | Molecular Brain | Full Text
ModelDB: NMDA receptors enhance the fidelity of synaptic integration (Li and Gulledge 2021)
ABLIM3 - hpluswiki
Paula Zamudio-bulcock's research topics | Profiles RNS
Keirstead, S. A.<...
Pravachol cost - Order The Cheapest medications online
Shunting Inhibition Does Not Have a Divisive Effect on Firing Rates* | Neural Computation | MIT Press
Pesquisa | Biblioteca Virtual em Saúde - BRASIL
Wheat germ agglutinin enhances EPSCs in cultured postnatal rat hippocampal neurons by blocking ionotropic quisqualate receptor...
GtR
Search Results For Health And Wellness: Peiion Results found: 24
Hiroshi Asanuma: H-index & Awards - Academic Profile | Research.com
ModelDB: Models that contain I Na,Ca
Qigong Institute
Profound deficits in hippocampal synaptic plasticity after traumatic brain injury and seizure is ameliorated by prophylactic...
"Central Suppression of Regenerated Proprioceptive Afferents" by Valerie K. Haftel, Edyta K. Bichler et al.
Neurons4
- In general, you can think of the pyramidal neurons as the excitatory ones, and the stellates as the inhibitory ones. (williamcalvin.com)
- Depolarization of membrane potentials at the SYNAPTIC MEMBRANES of target neurons during neurotransmission. (bvsalud.org)
- Excitatory synaptic transmission in many neurons is mediated by two co-expressed ionotropic glutamate receptor subtypes, AMPA and NMDA receptors, that differ in their kinetics, ion-selectivity, and voltage-sensitivity. (yale.edu)
- The effect of the lectin wheat germ agglutinin (WGA), an inhibitor of ionotropic quisqualate receptor desensitization, on both evoked and spontaneous fast excitatory postsynaptic events was examined in cultured postnatal rat hippocampal neurons with the use of whole cell recordings. (wustl.edu)
EPSPs2
- Here we report that the voltage-dependency and kinetics of NMDA receptors act synergistically to stabilize synaptic integration of excitatory postsynaptic potentials (EPSPs) across spatial and voltage domains. (yale.edu)
- They receive fast EPSPs (excitatory postsynaptic potentials) from neighbouring pyramids that exhibit paired pulse depression and display no ?sag? (ukri.org)
Synaptic potentials3
- Simultaneous paired recording were then used to calculate a correlation probability (CP) to infer the proportion of shared input based on the occurrence of simultaneous synaptic potentials. (nih.gov)
- Shu Y, Hasenstaub A, Duque A, Yu Y, McCormick DA (2006) Modulation of intracortical synaptic potentials by presynaptic somatic membrane potential. (yale.edu)
- When combined with AMPA conductance, the NMDA conductance balances voltage- and impedance-dependent changes in synaptic driving force, and distance-dependent attenuation of synaptic potentials arriving at the axon, to increase the fidelity of synaptic integration and EPSP-spike coupling across neuron state (i.e., initial membrane potential) and dendritic location of synaptic input. (yale.edu)
Neuron1
- On the other side of the synapse, the neurotransmitter causes (via that sniffer mechanism) a small voltage change in the downstream neuron known as an excitatory postsynaptic potential (EPSP). (williamcalvin.com)
Currents3
- WGA, at 580 nM, potentiated evoked fast excitatory postsynaptic currents (EPSCs) by increasing the amplitudes by 100 ± 27% (mean ± SE) and the time constant of decay from 5.8 ± 0.6 to 7.9 ± 0.5 ms. The increases in these parameters were not accompanied by changes in the current-voltage (I-V) relationship or pharmacological profile of the fast EPSCs. (wustl.edu)
- WGA did not alter the amplitude or time course of decay of inhibitory postsynaptic currents (IPSCs), and it did not alter neuronal input resistance or action potentials. (wustl.edu)
- GCs were exposed to barrages of fast AMPAR-mediated excitatory postsynaptic currents (EPSCs), primarily relayed from the entorhinal cortex, and inhibitory postsynaptic currents (IPSCs), presumably generated by local interneurons. (qigonginstitute.org)
Inhibitory1
- In addition, at distal synapses, shunting inhibition will also have an approximately subtractive effect if the excitatory conductance is not small compared to the inhibitory conductance. (mit.edu)
Presynaptic4
- Intracortical synaptic potential modulation by presynaptic somatic potential (Shu et al. (yale.edu)
- 1993). Fluctuations in pyramid-pyramid excitatory postsynaptic potentials modified by presynaptic firing pattern and postsynaptic membrane potential using paired intracellular recordings in rat neocortex. (modeldb.science)
- Electrophysiological (ePhys) studies including paired-pulse stimulation for short-term presynaptic plasticity and long-term potentiation (LTP) of CA1 Schaffer collateral synapses of the hippocampus for postsynaptic function survey were followed at post-event 1 hour, 3 and 7 days respectively. (tmu.edu.tw)
- Conclusion: Our data indicates that synaptic plasticity (i.e., both presynaptic and postsynaptic) suppression occurs in TBI followed by a seizure and that the interval between the TBI and seizure is an important factor in the severity of the resulting deficits. (tmu.edu.tw)
Receptors4
- Polysynaptic excitatory postsynaptic potentials that trigger spasms after spinal cord injury in rats are inhibited by 5-HT1B and 5-HT1F receptors. (rndsystems.com)
- AMPA receptors have fast kinetics and are voltage-insensitive, while NMDA receptors have slower kinetics and increased conductance at depolarized membrane potentials. (yale.edu)
- We will therefore test the hypothesis that the long, horizontally oriented dendrites of CA2 interneurones express HCN subunits and postsynaptic receptors and receive excitatory inputs that are distinct from those of their vertically oriented dendrites in SR and SLM. (ukri.org)
- We will employ dual and triple intracellular recordings to compare inputs to CA2 interneurones from pyramids in CA1, CA2 and CA3, manipulate Ih and postsynaptic receptors pharmacologically, reveal cellular markers and the localization of HCN subunits and postsynaptic receptors in these biocytin-labelled cells using confocal immuno-fluorescence and identify the locations of recorded synapses histologically. (ukri.org)
Membrane3
- Simulations of synaptic integration in simplified and morphologically realistic dendritic trees revealed that the combined presence of AMPA and NMDA conductances reduces the variability of somatic responses to spatiotemporal patterns of excitatory synaptic input presented at different initial membrane potentials and/or in different dendritic domains. (yale.edu)
- This moderating effect of the NMDA conductance on synaptic integration was robust across a wide range of AMPA-to-NMDA ratios, and results from synergistic interaction of NMDA kinetics (which reduces variability across membrane potential) and voltage-dependence (which favors stabilization across dendritic location). (yale.edu)
- Averaged over several interspike intervals, the spiking mechanism effectively clamps the somatic membrane potential to a value significantly above the resting potential, so that the current through the shunting conductance is approximately independent of the firing rate. (mit.edu)
Synapses1
- Insights Into the Role of the astroglial network that allows for better diffusion of glutamate released at synapses, leading to impaired excitatory synaptic transmission and induction of LTP, which translated into a loss of contextual fear memory pravachol cost. (perpetually49.com)
Amplitudes1
- Shunting inhibition, a conductance increase with a reversal potential close to the resting potential of the cell, has been shown to have a divisive effect on subthreshold excitatory postsynaptic potential amplitudes. (mit.edu)
Dendritic1
- Selective activation of BK channels in small-headed dendritic spines suppresses excitatory postsynaptic potentials. (yale.edu)
Inputs1
- Whether an individual neurone responds to a complex input pattern is determined by the strength of its excitatory inputs at that moment, its state at that time and importantly, by the inhibition it receives. (ukri.org)
Glutamate1
- This directly reduced synaptic glutamate concentration, hippocampal excitatory synaptic transmission in mice with normal or upregulated pravachol cost Cx30 expression. (perpetually49.com)
IPSCs1
- EPSCs exhibited coherence with the field potential predominantly in the theta frequency band, whereas IPSCs showed coherence primarily in the gamma range. (qigonginstitute.org)
Trigger1
- Excitatory postsynaptic potentials can singly or in summation reach the trigger threshold for ACTION POTENTIALS. (bvsalud.org)
Pyramidal1
- Properties of action potential initiation in neocortical pyramidal cells: evidence from whole cell axon recordings. (yale.edu)
Axon1
- Release of neurotransmitter happens when a brief electrical impulse (also known as a spike or action potential) is sent from the beginning of the axon near the cell body. (williamcalvin.com)
Mechanism1
- These results suggest that WGA augments hippocampal excitatory postsynaptic events via a postsynaptic mechanism. (wustl.edu)
Fast1
- The results further imply that ionotropic quisqualate receptor desensitization can modulate the amplitude and time course of decay of fast excitatory synaptic events. (wustl.edu)
Sparse2
- On T1 (acquisition trial), subjects were placed back in the human microbiome and aging remains sparse, some initial observations highlight the potential to pair mechanistic and translational microbiome research and the probability of sexual reproduction with endemic blast fungus through functional losses in a substitution at position 143 in the. (perpetually49.com)
- GCs in vivo fired action potentials at low frequency, consistent with sparse coding in the dentate gyrus. (qigonginstitute.org)
Mice1
- Peripheral serotonin receptor 2B and transient receptor potential channel 4 mediate pruritus to serotonergic antidepressants in mice. (rndsystems.com)
Input1
- We characterized the functional excitatory local input to these 3 cell subtypes in rat primary visual cortex using laser-scanning photostimulation. (nih.gov)
Motor1
- Hiroshi Asanuma studied Motor cortex and Excitatory postsynaptic potential that intersect with Electrophysiology and Stimulation. (research.com)
Electrical1
- Muscle stretch failed to evoke detectable synaptic responses in 13 of 22 motoneurons, although electrical stimulation generated monosynaptic excitatory postsynaptic potentials that were indistinguishable from normal. (wright.edu)
State1
- In this study, an ultra-performance liquid chromatography-Q-Exactive hybrid quadrupole-Orbitrap mass spectrometry-based untargeted hippocampus high-throughput metabolomics method was first performed to screen for potential biomarkers in a schizophrenia-like state in a chronically administered ketamine-induced mouse model. (bvsalud.org)
Action potential1
- A dynamic model of the cardiac ventricular action potential. (modeldb.science)
Network1
- Action potentials in GCs were phase locked to network oscillations. (qigonginstitute.org)
Role1
- One particular aspect of synaptic plasticity that has seldom been explored is the role of noncoding regions of the genome and the potential regulatory functions that they contain. (frontiersin.org)