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NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD)

机译:NMDA受体依赖性的长期增强和长期抑制(LTP / LTD)

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摘要

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.
机译:可以通过激活N-甲基-d-天冬氨酸(NMDA)型谷氨酸受体来引起长期增强和长期抑制(LTP / LTD),通常是通过突触前和突触后神经元的同时活动来引起的。表达的早期阶段由AMPA型谷氨酸受体的重新分布介导:添加更多的受体以增强突触,或去除受体以减弱突触。随着时间的流逝,结构变化变得明显,这通常需要合成新的蛋白质。对这些形式的突触可塑性的分子和细胞机制的研究已引起广泛关注,因为NMDA受体依赖性LTP和LTD可能构成学习和记忆的细胞底物。

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