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Short-term synaptic enhancement results from an increased probability of synaptic terminals releasing transmitters in response to pre-synaptic action potentials. Synapses will strengthen for a short time because of an increase in the amount of packaged transmitter released in response to each action potential. [ 22 ]
PPF is thus a form of short-term synaptic plasticity. The mechanisms underlying neural facilitation are exclusively pre-synaptic; broadly speaking, PPF arises due to increased presynaptic Ca 2+ concentration leading to a greater release of neurotransmitter-containing synaptic vesicles. [1]
Klyachko V.A. and Stevens C.F. (2006) Temperature-dependent shift of balance among the components of short-term plasticity in hippocampal synapses. J. Neurosci. 26, 6945-6957. Magleby K.L. and Zengel J.E. (1976a) Augmentation: A process that acts to increase transmitter release at the frog neuromuscular junction. J. Physiol. 257, 449-470.
These changes are called synaptic plasticity and may result in either a decrease in the efficacy of the synapse, called depression, or an increase in efficacy, called potentiation. These changes can either be long-term or short-term. Forms of short-term plasticity include synaptic fatigue or depression and synaptic augmentation.
Synaptic fatigue, is seldom used, instead, it is called short-term synaptic depression, which is an activity-dependent form of short term synaptic plasticity that results in the temporary inability of neurons to fire and therefore transmit an input signal.
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 ...
These synaptic changes can clearly lead to modification in circuit function and to behavioral plasticity. Some patterns of synaptic activity produce an extensive increase in synaptic strength, also known as Long-Term Potentiation (LTP). In the hippocampus, LTP at Schaffer collateral-CA1 modulates the biophysical properties of AMPA receptors.
For example, when plastic changes lead to long-term depression, calcineurin is used. Conversely, when plasticity leads to long-term potentiation, CaMKII is used. [6] In order for synaptic plasticity to be input-specific, these synaptic tags are essential on post-synaptic targets, to ensure synaptic potentiation is localized. [6] These tags will ...