Huang C C, Tsai J J, Gean P W
Department of Pharmacology, College of Medicine, National Cheng-Kung University, Tainan City, Taiwan, ROC.
Neurosci Lett. 1993 Oct 29;161(2):207-10. doi: 10.1016/0304-3940(93)90295-v.
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 microM) and picrotoxin (50 microM) which block non-NMDA and GABAA receptors, respectively. Superfusion of Iso (15 microM) produced a sustained increase in EPSPNMDA. Rp-adenosine-3',5'-cyclic monophosphotioate (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 EPSNMDA. These results suggest that cAMP-dependent protein kinase mediates the enhancement of EPSPNMDA by Iso in the amygdala.
在大鼠杏仁核的体外脑片制备中，研究了异丙肾上腺素（Iso）对N-甲基-D-天冬氨酸（NMDA）受体介导的突触电位（EPSPNMDA）的促进作用的细胞内机制。在分别阻断非NMDA和GABAA受体的6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX，10微摩尔）和苦味毒（50微摩尔）存在的情况下，从基底外侧杏仁核神经元进行细胞内记录。Iso（15微摩尔）的灌流使EPSPNMDA持续增加。单独使用蛋白激酶A（PKA）的强效抑制剂Rp-腺苷-3',5'-环磷酸硫酯（Rp-cAMPS）可使EPSPNMDA的幅度降至基线值以下，并阻止随后Iso引起的增强作用。腺苷酸环化酶的直接激活剂福斯高林模拟了Iso的作用，Rp-cAMPS也可逆转福斯高林诱导的EPSNMDA增强。这些结果表明，cAMP依赖性蛋白激酶介导了Iso对杏仁核中EPSPNMDA的增强作用。
