NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD)
NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD)
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DOI：
10.1101/cshperspect.a005710
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发表时间：
2012-06-01
影响因子：
7.2
通讯作者：
Malenka, Robert C.
中科院分区：
文献类型：
--
作者：
Luescher, Christian;Malenka, Robert C.
长时程增强和长时程抑制(LTP/LTD)可通过激活N-甲基-D-天冬氨酸(NMDA)型谷氨酸受体而引起，通常是由突触前和突触后神经元的一致活动引起的。表达的早期阶段是由AMPA型谷氨酸受体的重新分布所介导的：增加更多的受体来加强突触，或者移除受体来削弱突触。随着时间的推移，结构变化变得明显，这通常需要合成新的蛋白质。对这些形式突触可塑性的分子和细胞机制的研究受到了极大的关注，因为NMDA受体依赖的LTP和LTD可能构成学习和记忆的细胞底物。
Long-term potentiation and long-term depression (LTP/LTD) can be elicited by activating N-methyl-D-aspartate (NMDA)-type glutamate receptors, typically by the coincident activity of pre- and postsynaptic neurons. The early phases of expression are mediated by a redistribution of AMPA-type glutamate receptors: More receptors are added to potentiate the synapse or receptors are removed to weaken synapses. With time, structural changes become apparent, which in general require the synthesis of new proteins. The investigation of the molecular and cellular mechanisms underlying these forms of synaptic plasticity has received much attention, because NMDA receptor-dependent LTP and LTD may constitute cellular substrates of learning and memory.