Excitatory postsynaptic potential

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Excitatory postsynaptic potentials
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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.


EPSPs in living cells are caused chemically. When an active presynaptic cell releases

excitatory postsynaptic current. This depolarizing current causes an increase in membrane potential, the EPSP.[1]

Excitatory molecules

The neurotransmitter most often associated with EPSPs is the

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

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).

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

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

GABA
and others may also be released and further complicate the interpretation.

See also

References

  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. PMID 10736372
    .
  3. PMID 8833454
    .
  4. S2CID 35749805
    .
  5. ^ "The neuronal genome of Caenorhabditis elegans". www.wormbook.org.
  6. 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

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