Asztély F, Gustafsson B
Institute of Physiology, Göteborg University, Sweden.
Mol Neurobiol. 1996 Feb;12(1):1-11. doi: 10.1007/BF02740744.
In the brain, most fast excitatory synaptic transmission is mediated through L-glutamate acting on postsynaptic ionotropic glutamate receptors. These receptors are of two kinds--the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate (non-NMDA) and the N-methyl-D-aspartate (NMDA) receptors, which are thought to be colocalized onto the same postsynaptic elements. This excitatory transmission can be modulated both upward and downward, long-term potentiation (LTP) and long-term depression (LTD), respectively. Whether the expression of LTP/LTD is pre-or postsynaptically located (or both) remains an enigma. This article will focus on what postsynaptic modifications of the ionotropic glutamate receptors may possibly underly long-term potentiation/depression. It will discuss the character of LTP/ LTD with respect to the temporal characteristics and to the type of changes that appears in the non-NMDA and NMDA receptor-mediated synaptic currents, and what constraints these findings put on the possible expression mechanism(s) for LTP/LTD. It will be submitted that if a modification of the glutamate receptors does underly LTP/LTD, an increase/ decrease in the number of functional receptors is the most plausible alternative. This change in receptor number will have to include a coordinated change of both the non-NMDA and the NMDA receptors.
在大脑中,大多数快速兴奋性突触传递是通过L-谷氨酸作用于突触后离子型谷氨酸受体介导的。这些受体有两种——α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)/海人藻酸(非NMDA)受体和N-甲基-D-天冬氨酸(NMDA)受体,它们被认为共定位于相同的突触后元件上。这种兴奋性传递可以分别向上和向下调节,即长期增强(LTP)和长期抑制(LTD)。LTP/LTD的表达是位于突触前还是突触后(或两者都有)仍然是一个谜。本文将重点探讨离子型谷氨酸受体的哪些突触后修饰可能是长期增强/抑制的基础。它将讨论LTP/LTD在时间特征方面以及在非NMDA和NMDA受体介导的突触电流中出现的变化类型方面的特征,以及这些发现对LTP/LTD可能的表达机制施加了哪些限制。有人认为,如果谷氨酸受体的修饰确实是LTP/LTD的基础,那么功能性受体数量的增加/减少是最合理的选择。受体数量的这种变化将必须包括非NMDA受体和NMDA受体的协同变化。