In neuroscience, an excitatory postsynaptic potential is a postsynaptic
potential that makes the 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, 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. EPSPs, like IPSPs, are graded. 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. 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 Excitatory graphs to the right need amendment as
the Threshold Potential is -55mV so the so-called failure would actually lead to
AP. The scale just needs altering to something more reasonable.
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 are mediated by the neurotransmitter acetylcholine, which is one of the
primary transmitters in the central nervous system of invertebrates. 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. Bernard Katz pioneered
the study of these mEPSPs at the neuromuscular junction 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. 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 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, figures are often given showing the field EPSP 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 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. 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
GABA Glycine
Nonspiking neurons Postsynaptic potential
References External links
Quantal transmission at neuromuscular synapses