Kamisaki Y, Hamahashi T, Mita C, Itoh T
Department of Clinical Pharmacology, Tottori University School of Medicine, Yonago, Japan.
J Pharmacol Exp Ther. 1991 Feb;256(2):634-8.
Release of endogenous Asp, Glu and gamma-aminobutyric acid (GABA) has been investigated using synaptosomes prepared from rat retina. Exposure in superfusion to a depolarizing concentration of KCl (30 mM) evoked overflow of Asp and Glu, which were almost entirely Ca-dependent. However, 70% of the GABA release was Ca-independent. Dopamine (DA) almost completely inhibited the K(+)-evoked release of Asp and Glu in a concentration-dependent manner, but the release of GABA was only partly inhibited. The potencies of DA (IC50) to Asp and Glu release were 12 and 30 nM, respectively. A selective D-2 receptor antagonist, S-sulpiride, counteracted the DA-induced inhibition of Asp and Glu release, but a selective D-1 antagonist, SCH 23390, showed no effect. The data suggest that D-2 dopamine receptors located on the Asp and Glu neurons in rat retina may inhibit the release of these excitatory amino acids.
利用从大鼠视网膜制备的突触体对内源性天冬氨酸(Asp)、谷氨酸(Glu)和γ-氨基丁酸(GABA)的释放进行了研究。在超灌流中暴露于去极化浓度的氯化钾(30 mM)会引起Asp和Glu的溢出,这几乎完全依赖于钙离子。然而,70%的GABA释放不依赖于钙离子。多巴胺(DA)以浓度依赖的方式几乎完全抑制了钾离子(K⁺)诱发的Asp和Glu释放,但GABA的释放仅受到部分抑制。DA(IC50)对Asp和Glu释放的效力分别为12 nM和30 nM。一种选择性D-2受体拮抗剂S-舒必利可抵消DA诱导的对Asp和Glu释放的抑制作用,但一种选择性D-1拮抗剂SCH 23390则无作用。这些数据表明,位于大鼠视网膜Asp和Glu神经元上的D-2多巴胺受体可能会抑制这些兴奋性氨基酸的释放。