期刊
NEUROPHARMACOLOGY
卷 39, 期 7, 页码 1274-1283出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0028-3908(99)00227-0
关键词
slow afterhyperpolarization; muscarinic; CA1 neurons; phosphatase; cGMP; cGMP-dependent protein kinase
The slow calcium-activated potassium current sI(AHP) underlies spike-frequency adaptation and has a substantial impact an the excitability of hippocampal CA1 pyramidal neurons. Among other neuromodulatory substances, sI(AHP) is modulated by acetylcholine acting via muscarinic receptors. The second-messenger systems mediating the suppression of sI(AHP) by muscarinic agonists are largely unknown. Both protein kinase C and A do not seem to be involved, whereas calcium calmodulin kinase II has been shown to take part in the muscarinic action on sI(AHP). We re-examined the mechanism of action of muscarinic agonists on sI(AHP) combining whole-cell recordings with the use of specific inhibitors or activators of putative constituents of the muscarinic pathway. Our results suggest that activation of muscarinic receptors reduces sI(AHP) in a G-protein-mediated and phospholipase C-independent manner. Furthermore, we obtained evidence for the involvement of the cGMP-cGK pathway and of a protein phosphatase in the cholinergic suppression of sI(AHP) whereas release of Ca2+ from IP3-sensitive stores seems to be relevant neither for maintenance nor for modulation of sI(AHP). (C) 2000 Elsevier Science Ltd. All rights reserved.
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