excitatory postsynaptic potential

興奮性シナプス後電位 EPSP

WordNet

1. existing in possibility; "a potential problem"; "possible uses of nuclear power" (同)possible
2. the inherent capacity for coming into being (同)potentiality, potency

PrepTutorEJDIC

1. 可能性のある,潜在的な / 可能性,潜在力 / 電位

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/04/28 16:31:36」(JST)

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[Wiki en表示]

This single EPSP does not sufficiently depolarize the membrane to generate an action potential.

The summation of these three EPSPs generates an action potential.

In neuroscience, an excitatory postsynaptic potential (EPSP) is a temporary depolarization of postsynaptic membrane potential caused by the flow of positively charged ions into the postsynaptic cell as a result of opening of ligand-gated ion channels. They are the opposite of inhibitory postsynaptic potentials (IPSPs), which usually result from the flow of negative ions into the cell or positive ions out of the cell. A postsynaptic potential is defined as excitatory if it makes the neuron more likely to fire an action potential. EPSPs can also result from a decrease in outgoing positive charges, while IPSPs are sometimes caused by an increase in positive charge outflow. The flow of ions that causes an EPSP is an excitatory postsynaptic current (EPSC).

EPSPs, like IPSPs, are graded (i.e. they have an additive effect). When multiple EPSPs occur on a single patch of postsynaptic membrane, their combined effect is the sum of the individual EPSPs. Larger EPSPs result in greater membrane depolarization and thus increase the likelihood that the postsynaptic cell reaches the threshold for firing an action potential.

Overview

EPSPs in living cells are caused chemically. When an active presynaptic cell releases neurotransmitters into the synapse, some of them bind to receptors on the postsynaptic cell. Many of these receptors contain an ion channel capable of passing positively charged ions either into or out of the cell (such receptors are called ionotropic receptors). At excitatory synapses, the ion channel typically allows sodium into the cell, generating an excitatory postsynaptic current. This depolarizing current causes an increase in membrane potential, the EPSP.

Excitatory molecules

The neurotransmitter most often associated with EPSPs is the amino acid glutamate, and is the main excitatory neurotransmitter in the central nervous system of vertebrates. Its ubiquity at excitatory synapses has led to it being called the excitatory neurotransmitter. In some invertebrates, glutamate is the main excitatory transmitter at the neuromuscular junction. In the neuromuscular junction of vertebrates, EPP (end-plate potentials) are mediated by the neurotransmitter acetylcholine, which is also the main transmitter in the central nervous system of invertebrates.^{[citation needed]} At the same time, GABA is the most common neurotransmitter associated with IPSPs in the brain. However, classifying neurotransmitters as such is technically incorrect, as there are several other synaptic factors that help determine a neurotransmitter's excitatory or inhibitory effects.

Miniature EPSPs and quantal analysis

The release of neurotransmitter vesicles from the presynaptic cell is probabilistic. In fact, even without stimulation of the presynaptic cell, a single vesicle will occasionally be released into the synapse, generating miniature EPSPs (mEPSPs). Bernard Katz pioneered the study of these mEPSPs at the neuromuscular junction (often called miniature end-plate potentials) in 1951, revealing the quantal nature of synaptic transmission. Quantal size can then be defined as the synaptic response to the release of neurotransmitter from a single vesicle, while quantal content is the number of effective vesicles released in response to a nerve impulse.^{[citation needed]} Quantal analysis refers to the methods used to deduce, for a particular synapse, how many quanta of transmitter are released and what the average effect of each quantum is on the target cell, measured in terms of amount of ions flowing (charge) or change in the membrane potential.

Field EPSPs

EPSPs are usually recorded using intracellular electrodes. The extracellular signal from a single neuron is extremely small and thus next to impossible to record in the human brain. However, in some areas of the brain, such as the hippocampus, neurons are arranged in such a way that they all receive synaptic inputs in the same area. Because these neurons are in the same orientation, the extracellular signals from synaptic excitation don't cancel out, but rather add up to give a signal that can easily be recorded with a field electrode. This extracellular signal recorded from a population of neurons is the field potential. In studies of hippocampal long-term potentiation (LTP), figures are often given showing the field EPSP (fEPSP) in stratum radiatum of CA1 in response to Schaffer collateral stimulation. This is the signal seen by an extracellular electrode placed in the layer of apical dendrites of CA1 pyramidal neurons. The Schaffer collaterals make excitatory synapses onto these dendrites, and so when they are activated, there is a current sink in stratum radiatum: the field EPSP. The voltage deflection recorded during a field EPSP is negative-going, while an intracellularly recorded EPSP is positive-going. This difference is due to the relative flow of ions (primarily the sodium ion) into the cell, which, in the case of the field EPSP is away from the electrode, while for an intracellular EPSPs it is towards the electrode. After a field EPSP, the extracellular electrode may record another change in electrical potential named the population spike which corresponds to the population of cells firing action potentials (spiking). In other regions than CA1 of the hippocampus, the field EPSP may be far more complex and harder to interpret as the source and sinks are far less defined. In regions such as the striatum, neurotransmitters such as dopamine, acetylcholine, GABA and others may also be released and further complicate the interpretation.

See also

• Inhibitory postsynaptic potential (IPSP)
• GABA
• Glycine
• Nonspiking neurons
• Postsynaptic potential

References

External links

• Quantal transmission at neuromuscular synapses

UpToDate Contents

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• 5. ベンゾジアゼピンの中毒および離脱 benzodiazepine poisoning and withdrawal

English Journal

• Synaptic energy drives the information processing mechanisms in spiking neural networks.

• El Laithy K, Bogdan M.Author information Faculty of Mathematics and Computer Science, Dept. of Computer Engineering, Leipzig University, Germany. kellaithy@informatik.uni-leipzig.de.AbstractFlow of energy and free energy minimization underpins almost every aspect of naturally occurring physical mechanisms. Inspired by this fact this work establishes an energy-based framework that spans the multi-scale range of biological neural systems and integrates synaptic dynamic, synchronous spiking activity and neural states into one consistent working paradigm. Following a bottom-up approach, a hypothetical energy function is proposed for dynamic synaptic models based on the theoretical thermodynamic principles and the Hopfield networks. We show that a synapse exposes stable operating points in terms of its excitatory postsynaptic potential as a function of its synaptic strength. We postulate that synapses in a network operating at these stable points can drive this network to an internal state of synchronous firing. The presented analysis is related to the widely investigated temporal coherent activities (cell assemblies) over a certain range of time scales (binding-by-synchrony). This introduces a novel explanation of the observed (poly)synchronous activities within networks regarding the synaptic (coupling) functionality. On a network level the transitions from one firing scheme to the other express discrete sets of neural states. The neural states exist as long as the network sustains the internal synaptic energy.
• Mathematical biosciences and engineering : MBE.Math Biosci Eng.2014 Apr 1;11(2):233-56. doi: 10.3934/mbe.2014.11. 233.
• Flow of energy and free energy minimization underpins almost every aspect of naturally occurring physical mechanisms. Inspired by this fact this work establishes an energy-based framework that spans the multi-scale range of biological neural systems and integrates synaptic dynamic, synchronous spiki
• PMID 24245716

• Effects of chronic stress in adolescence on learned fear, anxiety, and synaptic transmission in the rat prelimbic cortex.

• Negrón-Oyarzo I1, Pérez MÁ2, Terreros G2, Muñoz P3, Dagnino-Subiabre A4.Author information 1Laboratory of Behavioral Neurobiology, Department of Physiology, Faculty of Sciences, Universidad de Valparaíso, Valparaíso, Chile; Centro Interdisciplinario de Neurociencia de Valparaíso, Universidad de Valparaíso, Valparaíso, Chile.2Laboratory of Behavioral Neurobiology, Department of Physiology, Faculty of Sciences, Universidad de Valparaíso, Valparaíso, Chile.3Centro Interdisciplinario de Neurociencia de Valparaíso, Universidad de Valparaíso, Valparaíso, Chile.4Laboratory of Behavioral Neurobiology, Department of Physiology, Faculty of Sciences, Universidad de Valparaíso, Valparaíso, Chile. Electronic address: alexies.dagnino@uv.cl.AbstractThe prelimbic cortex and amygdala regulate the extinction of conditioned fear and anxiety, respectively. In adult rats, chronic stress affects the dendritic morphology of these brain areas, slowing extinction of learned fear and enhancing anxiety. The aim of this study was to determine whether rats subjected to chronic stress in adolescence show changes in learned fear, anxiety, and synaptic transmission in the prelimbic cortex during adulthood. Male Sprague Dawley rats were subjected to seven days of restraint stress on postnatal day forty-two (PND 42, adolescence). Afterward, the fear-conditioning paradigm was used to study conditioned fear extinction. Anxiety-like behavior was measured one day (PND 50) and twenty-one days (PND 70, adulthood) after stress using the elevated-plus maze and dark-light box tests, respectively. With another set of rats, excitatory synaptic transmission was analyzed with slices of the prelimbic cortex. Rats that had been stressed during adolescence and adulthood had higher anxiety-like behavior levels than did controls, while stress-induced slowing of learned fear extinction in adolescence was reversed during adulthood. As well, the field excitatory postsynaptic potentials of stressed adolescent rats had significantly lower amplitudes than those of controls, although the amplitudes were higher in adulthood. Our results demonstrate that short-term stress in adolescence induces strong effects on excitatory synaptic transmission in the prelimbic cortex and extinction of learned fear, where the effect of stress on anxiety is more persistent than on the extinction of learned fear. These data contribute to the understanding of stress neurobiology.
• Behavioural brain research.Behav Brain Res.2014 Feb 1;259:342-53. doi: 10.1016/j.bbr.2013.11.001. Epub 2013 Nov 8.
• The prelimbic cortex and amygdala regulate the extinction of conditioned fear and anxiety, respectively. In adult rats, chronic stress affects the dendritic morphology of these brain areas, slowing extinction of learned fear and enhancing anxiety. The aim of this study was to determine whether rats
• PMID 24216268

• Nicotine-induced impairments of spatial cognition and long-term potentiation in adolescent male rats.

• Han G, An L, Yang B, Si L, Zhang T.Author information 1College of Life Science, Nankai University, Tianjin, China.AbstractThe aim of the present study was to investigate whether cognitive behavioral impairment, induced by nicotine in offspring rats, was associated with the alteration of hippocampal short-term potentiation (STP) and long-term potentiation (LTP) and to discuss the potential underlying mechanism. Young adult offspring rats were randomly divided into three groups. The groups include: control group (CC), nicotine group 1 (NC), in which their mothers received nicotine from gestational day 3 (GD3) to GD18, and nicotine group 2 (CN), in which young adult offspring rats received nicotine from postnatal day 42 (PD42) to PD56. Morris water maze (MWM) test was performed and then field excitatory postsynaptic potentials elicited by the stimulation of perforant pathway were recorded in the hippocampal dentate gyrus region. The results of the MWM test showed that learning and memory were impaired by either prenatal or postnatal nicotine exposure. In addition, it was found that there was no statistical difference of the MWM data between both nicotine treatments. In the electrophysiological test, LTP and STP were significantly inhibited in both NC and CN groups in comparison with the CC group. Notably, STP in CN group was also lower than that in the NC group. These findings suggested that both prenatal and postnatal exposure to nicotine induced learning and memory deficits, while the potential mechanism might be different from each other due to their dissimilar impairments of synaptic plasticity.
• Human & experimental toxicology.Hum Exp Toxicol.2014 Feb;33(2):203-13. doi: 10.1177/0960327113494902. Epub 2013 Jul 8.
• The aim of the present study was to investigate whether cognitive behavioral impairment, induced by nicotine in offspring rats, was associated with the alteration of hippocampal short-term potentiation (STP) and long-term potentiation (LTP) and to discuss the potential underlying mechanism. Young ad
• PMID 23836840

Japanese Journal

• 神経発火の非同期化を介して起こる海馬てんかん様リズムの抑制

• 橋本 あゆみ,夏目 季代久
• 電子情報通信学会技術研究報告. NLP, 非線形問題 109(366), 85-90, 2010-01-14
• ラット海馬スライスを用いてpicrotoxin誘導てんかん様発火に対するアセチルコリン受容体活性化の影響について調べた。てんかん様発火の振幅はカルバコール濃度依存的に減少した。この結果は、アセチルコリン受容体の活性化が海馬錐体細胞の同期性を減少させたこと示唆している。さらに、カルバコールによってCA3領域リカレントネットワークにおける集合興奮性シナプス後電位(pEPSP)の振幅は減少した。これらの …
• NAID 110008001773

• Methylphenidate Enhances Inhibitory Synaptic Transmission by Increasing the Content of Norepinephrine in the Locus Coeruleus of Juvenile Rats

• KIDANI YURI,ISHIMATSU MASARU,AKASU TAKASHI
• The Kurume Medical Journal 57(1/2), 29-38, 2010
• … MPH (1 μM) enhanced the amplitude of the inhibitory postsynaptic potential (IPSP) mediated by norepinephrine (NE), but did not change the excitatory postsynaptic potential (EPSP) mediated by excitatory amino acids. …
• NAID 130000441578

Related Pictures

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★リンクテーブル★

リンク元	「興奮性シナプス後電位」
拡張検索	「field excitatory postsynaptic potential」
関連記事	「potential」「excitatory」「postsynaptic」「postsynaptic potential」

「興奮性シナプス後電位」

　　[★]

英

excitatory postsynaptic potential, EPSP (SP)

• シナプス後ニューロンの膜にある受容体に神経伝達物質が結合すると、その膜のイオン透過性が変わり、シナプス後電位が発生する。興奮性のシナプスではEPSPが発生し、それが活動電位の閾値を超すとインパルスが発生する(SP.129-130)

「field excitatory postsynaptic potential」

　　[★]

興奮性シナプス後場電位

関

fEPSP

「potential」

　　[★]

• n.

• 電位、可能性、ポテンシャル

• adj.

• 潜在的な、可能な、有望な

関

capability、capable、electric potential、electrical potential、feasibility、feasible、latently、likelihood、odds、possibility、possible、potentiality、potentially、probability、promising、voltage

　 　 　

「excitatory」

　　[★]

• 興奮性の、興奮の

関

excitability、excitable、excitation、excite、excitement、exciting、excito、fire

「postsynaptic」

　　[★]

• シナプス後の、後シナプスの、・ストシナプスの、シナプス後性の

関

postsynaptically

「postsynaptic potential」

　　[★]

• シナプス後電位

関

p.s.p.