Differential alteration of hippocampal synaptic strength induced by pituitary adenylate cyclase activating polypeptide-38 (PACAP-38)

被引：38

作者：

Kondo, T

Tominaga, T

Ichikawa, M

Iijima, T

机构：

[1] Supermolecular Science Division, Electrotechnical Laboratory, Tsukuba 305, 1-1-4, Umezono

[2] Pacific Biomedical Research Center, Department of Microbiology, University of Hawaii, Honolulu

来源：

NEUROSCIENCE LETTERS | 1997年 / 221卷 / 2-3期

关键词：

pituitary adenylate cyclase activating polypeptide-38; hippocampal slice; long-term potentiation; long-term depression; CA1; dentate gyrus; protein kinase inhibitors;

D O I：

10.1016/S0304-3940(96)13323-1

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

We investigated the effect of pituitary adenylate cyclase activating polypeptide-38 (PACAP-38) on synaptic transmission in rat hippocampal slices using extracellular recordings. Brief bath application of PACAP-38 induced a long-lasting depression of transmission at the Schaffer collateral-CA1 synapse while at the same time causing enhancement of the perforant path-granule cell synapse in the dentate gyrus. Depression at the CA1 synapse was not occluded by low frequency-induced long-term depression (LTD), nor was enhancement at the granule cell synapse blocked by previous high frequency-induced long-term potentiation (LTP). Both actions of PACAP-38 could be elicited in the presence of an N-methyl-D-aspartate (NMDA) receptor antagonist, or in the presence of inhibitors of cyclic AMP- or Ca2+-dependent protein kinases, suggesting a novel mechanism of synaptic modulation. (C) 1997 Elsevier Science Ireland Ltd.

引用

页码：189 / 192

页数：4

共 20 条

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