Audi E A, Graeff F G
Eur J Pharmacol. 1987 Mar 17;135(2):225-9. doi: 10.1016/0014-2999(87)90615-7.
Intracerebral injection of the GABAA agonists muscimol (1 nmol), isoguvacine (1 nmol) or THIP (1, 2 and 4 nmol) in rats with chemitrodes implanted in the dorsal midbrain central grey raised the threshold electrical current for inducing escape behaviour. The effect of THIP was dose-dependent. In contrast, the GABAB agonist baclofen (10 and 100 nmol) did not affect the aversive threshold. Furthermore, pretreatment with baclofen (10 nmol and 100 nmol) did not significantly change the effect of THIP (2 nmol). These results indicate that the antiaversive action of GABA in the midbrain central grey is mediated by GABAA but not by GABAB receptors.
在将化学微电极植入中脑中央灰质背侧的大鼠中,脑室内注射GABAA激动剂蝇蕈醇(1纳摩尔)、异鹅膏蕈氨酸(1纳摩尔)或 THIP(1、2和4纳摩尔)可提高诱发逃避行为的阈电流。THIP的作用呈剂量依赖性。相比之下,GABAB激动剂巴氯芬(10和100纳摩尔)不影响厌恶阈值。此外,用巴氯芬(10纳摩尔和100纳摩尔)预处理不会显著改变THIP(2纳摩尔)的作用。这些结果表明,中脑中央灰质中GABA的抗厌恶作用是由GABAA而非GABAB受体介导的。