NOVEL FORM OF LONG-TERM POTENTIATION PRODUCED BY A K+ CHANNEL BLOCKER IN THE HIPPOCAMPUS
NOVEL FORM OF LONG-TERM POTENTIATION PRODUCED BY A K+ CHANNEL BLOCKER IN THE HIPPOCAMPUS
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DOI：
10.1038/349067a0
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发表时间：
1991-01-03
期刊：
影响因子：
64.8
通讯作者：
BENARI, Y
中科院分区：
文献类型：
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作者：
ANIKSZTEJN, L;BENARI, Y
海马突触传递的长时程增强（LTP）是一种广泛研究的记忆过程模型1。 在CA 1区，LTP由CA 2+通过N-甲基-D-天冬氨酸（NMDA）受体通道进入触发，并由CA 2+敏感性细胞内信使的激活维持2，3。 我们现在报告，在CA 1中，I（C），I（M）和延迟整流（I（K））的四乙基铵的短暂阻断产生了Ca 2+依赖性NMDA非依赖性形式的LTP。 我们的研究结果表明，这种新形式的LTP（简称LTP（K））是由谷氨酸的瞬时增强释放引起的，谷氨酸的瞬时增强释放通过非NMDA受体产生去极化，并随后激活电压依赖性Ca ~（2+）通道。
LONG-term potentiation (LTP) of synaptic transmission in the hippocampus is a widely studied model of memory processes1. In the CA1 region, LTP is triggered by the entry of CA2+ through N-methyl-D-aspartate (NMDA) receptor channels and maintained by the activation of CA2+-sensitive intracellular messengers2,3. We now report that in CA1, a transient block by tetraethylammonium of I(C), I(M) and the delayed rectifier (I(K)) produces a Ca2+-dependent NMDA-independent form of LTP. Our results suggest that this new form of LTP (referred as to LTP(K)) is induced by a transient enhanced release of glutamate which generates a depolarization by way of the non-NMDA receptors and the consequent activation of voltage -dependent Ca2+ channels.