Enhancement of NMDA receptor-mediated synaptic potential by isoproterenol is blocked by Rp-adenosine 3′,5′-cyclic monophosphothioate

Chiung Chun Huang, Jing Jane Tsai, Po Wu Gean

研究成果: Article同行評審

29 引文 斯高帕斯(Scopus)

摘要

The intracellular mechanisms underlying the facilitatory action of isoproterenol (Iso) on the NMDA receptor-mediated synaptic potential (EPSPnmda) was investigated in an in vitro slice preparation of rat amygdala. Intracellular recordings were made from basolateral amygdala neurons in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 μM) and picrotoxin (50 μM) which block non-NMDA and GABAa receptors, respectively. Superfusion of Iso (15 μM) produced a sustained increase in EPSPnmda. Rp-adenosine-3′,5′-cyclic monophosphothioate (Rp-cAMPS), a potent inhibitor of protein kinase A (PKA) alone decreased the amplitude of EPSPnmda below baseline values and prevented the subsequent potentiation by Iso. Forskolin, a direct activator of adenylate cyclase, mimics the effect of Iso, and Rp-cAMPS also reversed forskolin-induced enhancement of EPSPnmda. These results suggest that cAMP-dependent protein kinase mediates the enhancement of EPSPnmda by Iso in the amygdala.

原文English
頁(從 - 到)207-210
頁數4
期刊Neuroscience Letters
161
發行號2
DOIs
出版狀態Published - 1993 10月 29

All Science Journal Classification (ASJC) codes

  • 神經科學 (全部)

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