Department of Pharmacology, Tokyo Dental College, Mihama-ku, Chiba 261-8502, Japan.
J Pharmacol Sci. 2010;112(2):247-50. doi: 10.1254/jphs.09269sc. Epub 2010 Jan 30.
We investigated the inhibitory role of gamma-aminobutyric acid A (GABA(A)) receptors on amylase release and the evidence for functional coupling with central-type benzodiazepine receptors in rat parotid acinar cells. Muscimol and GABA decreased isoprenaline-induced amylase release. This effect was blocked by bicuculline, a GABA(A)-receptor antagonist, and enhanced by clonazepam, a central-type benzodiazepine-receptor agonist, and diazepam, a central- and peripheral-type benzodiazepine-receptor agonist. Although bicuculline completely blocked the combination effect of GABA(A)-receptor agonist and clonazepam, it did not completely block the combination effect with diazepam. These results suggest that protein secretion is suppressively regulated by GABA(A) receptors coupled with central-type benzodiazepine receptors.
我们研究了γ-氨基丁酸 A(GABA(A))受体对大鼠腮腺细胞中淀粉酶释放的抑制作用,以及与中枢型苯二氮䓬受体功能偶联的证据。Musci mol 和 GABA 降低了异丙肾上腺素诱导的淀粉酶释放。这种作用被 GABA(A)受体拮抗剂 Bicuculline 阻断,被中枢型苯二氮䓬受体激动剂氯硝西泮和外周型和中枢型苯二氮䓬受体激动剂地西泮增强。尽管 Bicuculline 完全阻断了 GABA(A)受体激动剂和氯硝西泮的组合效应,但它并没有完全阻断与地西泮的组合效应。这些结果表明,蛋白质分泌受到与中枢型苯二氮䓬受体偶联的 GABA(A)受体的抑制性调节。