Audi E A, Graeff F G
Eur J Pharmacol. 1984 Aug 17;103(3-4):279-85. doi: 10.1016/0014-2999(84)90488-6.
The microinjection of 80, 160 and 320 nmol chlordiazepoxide (CDP) as well as of 20, 40 and 80 nmol midazolam (MDZ) into the dorsal midbrain of rats bearing chronically implanted chemitrodes raised the threshold electrical current inducing escape behaviour by stimulating the dorsal periaqueductal grey matter (DPAG). Parallel linear regressions were obtained by plotting the log dose against drug-induced increases in escape threshold, MDZ being 3.55 times more potent than CDP (95% confidence limits 1.21 and 8.57). Local pretreatment with 80 nmol of the benzodiazepine antagonist Ro 15-1788 blocked the anti-aversive effect of either 160 nmol CDP or 40 nmol MDZ. The same dose of Ro 15-1788 was ineffective when given alone. These results suggest that the anti-aversive action of CDP and MDZ is due to their combination with benzodiazepine receptors in the DPAG.
向长期植入化学微电极的大鼠中脑背侧微量注射80、160和320纳摩尔的氯氮卓（CDP）以及20、40和80纳摩尔的咪达唑仑（MDZ），通过刺激导水管周围灰质背侧（DPAG）提高了诱发逃避行为的阈电流。通过绘制对数剂量与药物诱导的逃避阈值增加量的关系图得到平行线性回归，MDZ的效力比CDP高3.55倍（95%置信区间为1.21和8.57）。用80纳摩尔苯二氮卓拮抗剂Ro 15 - 1788进行局部预处理可阻断160纳摩尔CDP或40纳摩尔MDZ的抗厌恶作用。相同剂量的Ro 15 - 1788单独给药时无效。这些结果表明，CDP和MDZ的抗厌恶作用是由于它们与DPAG中的苯二氮卓受体结合所致。
