G蛋白偶联受体控制海马体中的N-甲基-D-天冬氨酸受体（NMDARs）和神经元可塑性。
G protein-coupled receptors control NMDARs and metaplasticity in the hippocampus.
作者信息
MacDonald John F, Jackson Michael F, Beazely Michael A
机构信息
Department of Physiology, University of Toronto, Toronto, ON, Canada.
出版信息
Biochim Biophys Acta. 2007 Apr;1768(4):941-51. doi: 10.1016/j.bbamem.2006.12.006. Epub 2006 Dec 14.
Long-term potentiation (LTP) and long-term depression (LTD) are the major forms of functional synaptic plasticity observed at CA1 synapses of the hippocampus. The balance between LTP and LTD or "metaplasticity" is controlled by G-protein coupled receptors (GPCRs) whose signal pathways target the N-methyl-D-asparate (NMDA) subtype of excitatory glutamate receptor. We discuss the protein kinase signal cascades stimulated by Galphaq and Galphas coupled GPCRs and describe how control of NMDAR activity shifts the threshold for the induction of LTP.
长时程增强（LTP）和长时程抑制（LTD）是在海马体CA1突触处观察到的功能性突触可塑性的主要形式。LTP和LTD之间的平衡或“元可塑性”由G蛋白偶联受体（GPCR）控制，其信号通路靶向兴奋性谷氨酸受体的N-甲基-D-天冬氨酸（NMDA）亚型。我们讨论了由Gαq和Gαs偶联的GPCR刺激的蛋白激酶信号级联反应，并描述了对NMDAR活性的控制如何改变LTP诱导的阈值。
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