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Postsynaptic potentials are changes in the membrane potential of the postsynaptic terminal of a chemical synapse. Postsynaptic potentials are graded potentials , and should not be confused with action potentials although their function is to initiate or inhibit action potentials.
Synaptic potentials, unlike action potentials, degrade quickly as they move away from the synapse. This is the case for both excitatory and inhibitory postsynaptic potentials. Synaptic potentials are not static. The concept of synaptic plasticity refers to the changes in synaptic potential. [6]
Two molecular mechanisms for synaptic plasticity involve the NMDA and AMPA glutamate receptors. Opening of NMDA channels (which relates to the level of cellular depolarization) leads to a rise in post-synaptic Ca 2+ concentration and this has been linked to long-term potentiation, LTP (as well as to protein kinase activation); strong depolarization of the post-synaptic cell completely ...
Both the presynaptic and postsynaptic sites contain extensive arrays of molecular machinery that link the two membranes together and carry out the signaling process. In many synapses, the presynaptic part is located on the terminals of axons and the postsynaptic part is located on a dendrite or soma .
When the presynaptic terminal is electrically stimulated, an array of molecules embedded in the membrane are activated, and cause the contents of the vesicles to be released into the narrow space between the presynaptic and postsynaptic membranes, called the synaptic cleft.
The inactivation of presynaptic Ca 2+ channels after repeated action potentials also contributes to STD. [8] Depression and facilitation interact to create short-term plastic changes within neurons, and this interaction is called the dual-process theory of plasticity. Basic models present these effects as additive, with the sum creating the net ...
Plasticity in the brain affects the strength of neural connections and pathways. Nonsynaptic plasticity is a form of neuroplasticity that involves modification of ion channel function in the axon, dendrites, and cell body that results in specific changes in the integration of excitatory postsynaptic potentials and inhibitory postsynaptic potentials.
In 1973, M. M. Taylor [1] suggested that if synapses were strengthened for which a presynaptic spike occurred just before a postsynaptic spike more often than the reverse (Hebbian learning), while with the opposite timing or in the absence of a closely timed presynaptic spike, synapses were weakened (anti-Hebbian learning), the result would be an informationally efficient recoding of input ...