Excitatory postsynaptic potential

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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 postsynaptic

potential that makes the postsynaptic neuron more likely to fire an action potential. This
temporary depolarization of postsynaptic membrane potential, caused by the flow of
positively charged ions into the postsynaptic cell, is a result of opening ligand-gated ion
channels. These 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.
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.
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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.[1]

Contents

 1Excitatory molecules
 2Miniature EPSPs and quantal analysis
 3Field EPSPs
 4See also
 5References
 6External links

Excitatory molecules[edit]
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.
[2]
 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.[3][4] In the neuromuscular junction of vertebrates, EPP (end-
plate potentials) are mediated by the neurotransmitter acetylcholine, which (along with
glutamate) is one of the primary transmitters in the central nervous system of
invertebrates.[5] 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[edit]

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[6]) 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.[7]

Field EPSPs[edit]
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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. [8] 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[edit]
 Glycine
 Nonspiking neurons
 Summation (neurophysiology)

References[edit]
 1. ^ Takagi, Hiroshi. “Roles of Ion Channels in EPSP Integration
at Neuronal Dendrites.” Neuroscience Research, vol. 37, no.
3, 2000, pp. 167–171., doi:10.1016/s0168-0102(00)00120-6.
2. ^ Meldrum, BS (Apr 2000).  "Glutamate as a neurotransmitter
in the brain: review of physiology and pathology".  The Journal
of Nutrition.  130  (4S Suppl): 1007S–
15S. doi:10.1093/jn/130.4.1007s.  PMID  10736372.
3. ^ Keshishian, H; Broadie K; Chiba A; Bate M (1996). "The
Drosophila Neuromuscular Junction: A Model System for
Studying Synaptic Development and Function". Annu. Rev.
Neurosci. 19: 545–
575.  doi:10.1146/annurev.ne.19.030196.002553. PMID 8833
454.
4. ^ Samoilova, MV; Frolova, EV; Potapjeva, NN; Fedorova, IM;
Gmiro, VE; Magazanik, LG (September 1997). "Channel
blocking drugs as tools to study glutamate receptors in insect
muscles and molluscan neurons". Invertebrate
Neuroscience. 3  (2–3): 117–
126.  doi:10.1007/BF02480366. S2CID  35749805.
5. ^ "The neuronal genome of Caenorhabditis
elegans".  www.wormbook.org.
6. ^ Functionally, mEPSPs and miniature end-plate potentials
(mEPPs) are identical. The name end-plate potential is used
since Katz's studies were performed on the neuromuscular
junction, the muscle fiber component of which is commonly
called the motor end-plate.
7. ^ "2001-2002 M.R. Bauer Foundation Colloquium Series".
Bio.brandeis.edu. Retrieved 2014-01-22.
8. ^ Bliss, T. V., & Lomo, T. (1973). Long-lasting potentiation of
synaptic transmission in the dentate area of the anaesthetized
rabbit following stimulation of the perforant path. The Journal
of physiology, 232(2), 331–356.
doi:10.1113/jphysiol.1973.sp010273

External links[edit]
 Quantal transmission at neuromuscular synapses
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Physiology of the nervous system

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teralization of brain function

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 Auditory evoked potential
ential
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 Neurotransmission

 Chronaxie

 Membrane potential
short
 Action potential
term
 Postsynaptic potential 
o Excitatory

o Inhibitory

 Axoplasmic transport

 Neuroregeneration/Nerve regeneration

term  Neuroplasticity/Synaptic plasticity 

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