Excitatory postsynaptic potential
neuroscience, an excitatory postsynaptic potential (EPSP) is a temporary depolarization of postsynaptic membrane potentialcaused by the flow of positively charged ions into the postsynaptic cell. They are the opposite of inhibitory postsynaptic potentials (IPSPs), which usually result from the flow of "negative" ions into the cell. A postsynaptic potentialis defined as excitatory if it makes it easier for the neuron 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
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 channelcapable 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."'
The neurotransmitter most often associated with EPSPs is the
amino acid glutamate, and is the main excitatory neurotransmitter in the central nervous systemof 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. [cite journal |last=Keshishian |first=H|coauthors=Broadie K, Chiba A, Bate M | title=The Drosophila Neuromuscular Junction: A Model System for Studying Synaptic Development and Function| journal=Ann. Rev. Neurosci. |volume=19 |pages=545-75|year=1996] [cite journal|last=Samoilova |first=MV|coauthors= Frolova EP, Potapjeva NN, et al| title= Channel blocking drugs as tools to study glutamate receptors in insect muscles and molluscan neurons| journal=Invert. Neurosci. |volume=3 |pages=117-26 |year=1997] In the neuromuscular junctionof vertebrates, EPP ( end-plate potentials) are mediated by the neurotransmitter acetylcholine, which is also the main transmitter in an invertebrates´ central nervous system. 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.
The release of neurotransmitter vesicles from the presynaptic cell is probabilistic. In fact, even without stimulation of the presynaptic cell, vesicles will occasionally be released into the synapse, generating EPSPs.
Bernard Katzpioneered the study of these spontaneous EPSPs (often called miniature end-plate potentials [Functionally, EPSPs and miniature end-plate potentials (mEPPs) are identical. The name "end-plate potential" is used since Katz' studies were performed on the neuromuscular junction, the muscle fibercomponent of which is commonly called the " motor end-plate".] ) in 1951, revealing the quantalnature 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.
EPSPs are usually recorded using intracellular electrodes. The extracellular signal from a single neuron is extremely small and thus next to impossible to record. 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 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 spikewhich 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 striatumneurotransmitters such as dopamine, acetylcholine, GABAand others may also be released and further complicate the interpretation.
Inhibitory postsynaptic potential
* [http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowSection&rid=neurosci.section.323 Quantal transmission at neuromuscular synapses]
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