腺苷受体激动剂可抑制缺血大鼠大脑皮质中γ-氨基丁酸（GABA）的释放。

Adenosine receptor agonists inhibit the release of gamma-aminobutyric acid (GABA) from the ischemic rat cerebral cortex.

作者信息

O'Regan M H, Simpson R E, Perkins L M, Phillis J W

机构信息

Department of Physiology, School of Medicine, Wayne State University, Detroit, MI 48201.

出版信息

Brain Res. 1992 Jun 5;582(1):22-6. doi: 10.1016/0006-8993(92)90312-w.

DOI:10.1016/0006-8993(92)90312-w

PMID:1498681

Abstract

The effects of CPA (a selective A1 receptor agonist), NECA (a mixed A1 and A2 receptor agonist), and CGS 21680 (a selective A2 receptor agonist) on the ischemia-evoked release of gamma-aminobutyric acid (GABA) from rat cerebral cortex was investigated with the cortical cup technique. Cerebral ischemia (20 min) was elicited by four vessel occlusion. In control animals, superfusate GABA increased from a basal level of 206 +/- 26 nM (mean +/- S.E.M., n = 18) to 10,748 +/- 3,876 nM during the reperfusion period. Pretreatment with adenosine receptor agonists failed to affect basal levels of GABA release. However, CPA (10(-10) M), NECA (10(-9) M), and CGS 21680 (10(-8) M) significantly suppressed the ischemia-evoked release of GABA. The ability to block the ischemia-evoked release of GABA was not evident when the adenosine receptor agonists were administered at higher concentrations. Thus, the selective activation of either A1 or high-affinity A2a adenosine receptors results in an inhibition of ischemia-evoked GABA release.

摘要

采用皮质杯技术研究了CPA（一种选择性A1受体激动剂）、NECA（一种A1和A2受体混合激动剂）和CGS 21680（一种选择性A2受体激动剂）对大鼠大脑皮质缺血诱发的γ-氨基丁酸（GABA）释放的影响。通过四动脉闭塞诱导脑缺血（20分钟）。在对照动物中，再灌注期间灌流液中的GABA从基础水平206±26 nM（平均值±标准误，n = 18）增加到10,748±3,876 nM。用腺苷受体激动剂预处理未能影响GABA释放的基础水平。然而，CPA（10^-10 M）、NECA（10^-9 M）和CGS 21680（10^-8 M）显著抑制了缺血诱发的GABA释放。当以较高浓度给予腺苷受体激动剂时，阻断缺血诱发的GABA释放的能力不明显。因此，选择性激活A1或高亲和力A2a腺苷受体可抑制缺血诱发的GABA释放。