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Anandamide, a naturally-occurring agonist of the cannabinoid receptor, blocks adenylate cyclase at the frog neuromuscular junction.

作者信息

Van der Kloot W

机构信息

Department of Physiology & Biophysics, SUNY, Stony Brook 11794-8661.

出版信息

Brain Res. 1994 Jun 27;649(1-2):181-4. doi: 10.1016/0006-8993(94)91062-6.

Abstract

Anandamide (arachydonylethanolamide) is a naturally-occurring ligand of the canabinoid receptor. When anandamide binds to its receptor, adenylate cyclase is inhibited. At the frog neuromuscular junction, anandamide lessened the increase in quantal size produced by pretreatment in hypertonic solution. It did not alter the increases in quantal size produced by insulin or by a permeable agonist of cAMP. It was known that hypertonic treatment increases quantal size by way of the cAMP-protein kinase A pathway. Anandamide had no effect on miniature endplate potential frequency (fmepp) in untreated preparations. After fmepp was increased in the presence of a permeable cAMP agonist, anandamide brought fmepp back to resting levels. The conclusions are that the motor nerve terminal has a cannabinoid receptor. The binding of anandamide to this receptor seems to block adenylate cyclase.

摘要

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