GABA-B AUTORECEPTORS REGULATE THE INDUCTION OF LTP
GABA-B AUTORECEPTORS REGULATE THE INDUCTION OF LTP
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DOI：
10.1038/349609a0
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发表时间：
1991-02-14
期刊：
影响因子：
64.8
通讯作者：
COLLINGRIDGE, GL
中科院分区：
文献类型：
--
作者：
DAVIES, CH;STARKEY, SJ;COLLINGRIDGE, GL
了解长时程增强（LTP）的机制将有助于深入了解脊椎动物学习和记忆的细胞和分子基础1。已经确定，在海马的CA 1区，LTP的诱导需要N-甲基-D-天冬氨酸（NMDA）受体系统的瞬时激活21。在低频传输过程中，γ-氨基丁酸（GABA）介导的突触抑制阻止了该系统的显著激活3，4，该突触抑制使神经元超极化至NMDA受体操纵的通道基本上被Mg 2+阻断的区域（参考文献3，4）。第5、6段）。但是在高频传导过程中，诱发的机制提供了足够的突触后膜去极化，以减少这种阻滞，从而允许LTP的诱导。我们现在报告说，这种关键的去极化是能够实现的，因为在高频传输过程中，GABA通过对GABA（B）自身受体的作用抑制其自身的释放，这允许足够的NMDA受体激活以诱导LTP。这些发现证明了GABA（B）受体在突触可塑性中的作用。
UNDERSTANDING the mechanisms involved in long-term potentiation (LTP) should provide insights into the cellular and molecular basis of learning and memory in vertebrates 1. It has been established that in the CA1 region of the hippocampus the induction of LTP requires the transient activation of the N-methyl-D-aspartate (NMDA) receptor system 21. During low-frequency transmission, significant activation of this system is prevented by gamma-aminobutyric acid (GABA) mediated synaptic inhibition 3,4 which hyperpolarizes neurons into a region where NMDA receptor-operated channels are substantially blocked by Mg2+ (refs. 5, 6). But during high-frequency transmission, mechanisms are evoked that provide sufficient depolarization of the postsynaptic membrane to reduce this block 7 and thereby permit the induction of LTP. We now report that this critical depolarization is enabled because during high-frequency transmission GABA depresses its own release by an action on GABA(B) autoreceptors, which permits sufficient NMDA receptor activation for the induction of LTP. These findings demonstrate a role for GABA(B) receptors in synaptic plasticity.