Department Neurobiology, Harvard Medical School, Boston, MA 02115, United States.
Curr Opin Neurobiol. 2011 Apr;21(2):269-74. doi: 10.1016/j.conb.2011.02.003. Epub 2011 Feb 23.
Synapses exhibit several forms of short-term plasticity that play a multitude of computational roles. Short-term depression suppresses neurotransmitter release for hundreds of milliseconds to tens of seconds; facilitation and post-tetanic potentiation lead to synaptic enhancement lasting hundreds of milliseconds to minutes. Recent advances have provided insight into the mechanisms underlying these forms of plasticity. Vesicle depletion, as well as inactivation of both release sites and calcium channels, contribute to synaptic depression. Mechanisms of short-term enhancement include calcium channel facilitation, local depletion of calcium buffers, increases in the probability of release downstream of calcium influx, altered vesicle pool properties, and increases in quantal size. Moreover, there is a growing appreciation of the heterogeneity of vesicles and release sites and how they can contribute to use-dependent plasticity.
突触表现出多种形式的短期可塑性，这些可塑性在计算中发挥着多种作用。短期抑制会在数百毫秒至数十秒内抑制神经递质的释放；易化和强直后增强则会导致持续数百毫秒至数分钟的突触增强。最近的研究进展为这些形式的可塑性的机制提供了深入的了解。囊泡耗竭，以及释放位点和钙通道的失活，都有助于突触抑制。短期增强的机制包括钙通道易化、钙缓冲剂的局部耗竭、钙内流下游释放概率的增加、囊泡库特性的改变以及量子大小的增加。此外，人们越来越认识到囊泡和释放位点的异质性，以及它们如何有助于依赖使用的可塑性。
