Van der Kloot W
Department of Physiology & Biophysics, SUNY, Stony Brook 11794-8661.
Brain Res. 1994 Jun 27;649(1-2):181-4. doi: 10.1016/0006-8993(94)91062-6.
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.
花生四烯酸乙醇胺是大麻素受体的一种天然存在的配体。当花生四烯酸乙醇胺与其受体结合时,腺苷酸环化酶会受到抑制。在青蛙神经肌肉接头处,花生四烯酸乙醇胺减弱了高渗溶液预处理所产生的量子大小增加。它并未改变胰岛素或cAMP可渗透激动剂所产生的量子大小增加。已知高渗处理通过cAMP - 蛋白激酶A途径增加量子大小。花生四烯酸乙醇胺对未处理制剂中的微小终板电位频率(fmepp)没有影响。在可渗透的cAMP激动剂存在下fmepp增加后,花生四烯酸乙醇胺使fmepp恢复到静息水平。结论是运动神经末梢有一个大麻素受体。花生四烯酸乙醇胺与该受体的结合似乎会阻断腺苷酸环化酶。