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N-甲基-D-天冬氨酸和使君子氨酸通过一种蛋白激酶介导的机制降低钙依赖性钾电流。

NMDA and quisqualate reduce a Ca-dependent K+ current by a protein kinase-mediated mechanism.

作者信息

Baskys A, Bernstein N K, Barolet A W, Carlen P L

机构信息

Playfair Neuroscience Unit, Toronto Western Hospital, Canada.

出版信息

Neurosci Lett. 1990 Apr 20;112(1):76-81. doi: 10.1016/0304-3940(90)90325-4.

DOI:10.1016/0304-3940(90)90325-4
PMID:2200979
Abstract

Stimulation of N-methyl-D-aspartate (NMDA) or quisqualate (Quis) receptors by submicromolar concentrations of NMDA or Quis but not alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) reduced post-spike train after hyperpolarizations (AHPs) and blocked the underlying Iahp in dentate granule (DG) neurones in vitro. The NMDA but not Quis action was blocked by the NMDA receptor blocker 2-D,L-aminophosphonovaleric acid (APV). Actions of both NMDA and Quis were abolished by isoquinolinesulphonyl-2-methyl-piperazine dihydrochloride (H-7), an inhibitor of several protein kinases. These data suggest that there is a link between excitatory amino acid receptor activation, the protein kinase system, and neuronal excitability.

摘要

亚微摩尔浓度的N-甲基-D-天冬氨酸(NMDA)或喹啉酸(Quis)而非α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)对NMDA或Quis受体的刺激,减少了峰电位后超极化(AHPs),并在体外阻断了齿状颗粒(DG)神经元中潜在的Iahp。NMDA受体阻滞剂2-D,L-氨基磷酸戊酸(APV)可阻断NMDA而非Quis的作用。几种蛋白激酶的抑制剂异喹啉磺酰-2-甲基-哌嗪二盐酸盐(H-7)可消除NMDA和Quis的作用。这些数据表明,兴奋性氨基酸受体激活、蛋白激酶系统和神经元兴奋性之间存在联系。

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NMDA and quisqualate reduce a Ca-dependent K+ current by a protein kinase-mediated mechanism.N-甲基-D-天冬氨酸和使君子氨酸通过一种蛋白激酶介导的机制降低钙依赖性钾电流。
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