POTASSIUM AND CALCIUM-CHANNEL INVOLVEMENT IN INDUCTION OF LONG-LASTING SYNAPTIC ENHANCEMENT BY CALYCULIN-A, A PROTEIN PHOSPHATASE INHIBITOR, IN RAT HIPPOCAMPAL CA1 REGION

被引：6

作者：

MURAKAMI, N ^{[1
]}

SAKAI, N ^{[1
]}

NEI, K ^{[1
]}

MATSUYAMA, S ^{[1
]}

SAITO, N ^{[1
]}

TANAKA, C ^{[1
]}

机构：

[1] KOBE UNIV,SCH MED,DEPT PHARMACOL,KOBE 650,JAPAN

来源：

NEUROSCIENCE LETTERS | 1994年 / 176卷 / 02期

关键词：

CALCIUM CHANNEL; CALYCULIN A; GLUTAMATE; HIPPOCAMPUS; LONG-TERM POTENTIATION; PLASTICITY; POTASSIUM CHANNEL; PROTEIN PHOSPHATASE;

D O I：

10.1016/0304-3940(94)90077-9

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

In the Schaffer collateral-CAl pathway in rat hippocampal slices, exposure to calyculin A induced a long-lasting potentiation of the extracellular held potentials with a transient increase in glutamate release. The synaptic enhancement produced by calyculin A was blocked by staurosporine and nicardipine, but not by D,L-2-amino-5-phosphonovalerate. In dissociated CAI pyramidal cells, calyculin A blocked the action-potential repolarization and fast after-hyperpolarization, and increased spike frequency. These results suggest that calyculin A-induced long-lasting potentiation is triggered by the blockade of Ca2+-activated K+ channels, the transient increase of glutamate release and the consequent activation of voltage-gated Ca2+ channels, and is maintained by increases in protein kinases activities.

引用

页码：181 / 184

页数：4

共 17 条

[1] NOVEL FORM OF LONG-TERM POTENTIATION PRODUCED BY A K+ CHANNEL BLOCKER IN THE HIPPOCAMPUS [J].