Voronin Leon L, Cherubini Enrico
Brain Research Institute, Academy of Medical Sciences and Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Butlerova str. 5a, 117485 Moscow, Russia.
Neuropharmacology. 2003 Sep;45(4):439-49. doi: 10.1016/s0028-3908(03)00173-4.
Conversion of "silent" synapses into active ones is a likely mechanism for long-term potentiation (LTP), an experimental paradigm for studying information storage. A widely accepted mechanism that has been suggested for synaptic silence is that functional AMPA glutamate receptors (AMPARs) are absent on the subsynaptic membrane. Evidence is presented here that in many cases the cause of apparent "silence" is presynaptic and due to a low level of glutamate release. Increased transmitter release is crucial for early LTP maintenance. Delayed modifications in postsynaptic receptors matched with transmitter release changes underlie structural alterations associated with late LTP phases.
“沉默”突触向活跃突触的转化可能是长时程增强（LTP）的一种机制，LTP是一种用于研究信息存储的实验范式。一种被广泛接受的关于突触沉默的机制是，突触后膜上不存在功能性的α-氨基-3-羟基-5-甲基-4-异恶唑丙酸型谷氨酸受体（AMPARs）。本文提供的证据表明，在许多情况下，明显“沉默”的原因是突触前的，且是由于谷氨酸释放水平较低。递质释放增加对于早期LTP维持至关重要。突触后受体的延迟修饰与递质释放变化相匹配，是晚期LTP阶段相关结构改变的基础。
