Sullivan R M, Henke P G, Ray A, Hebert M A, Trimper J M
St. Francis Xavier University, Antigonish, Nova Scotia, Canada.
Behav Neural Biol. 1989 Mar;51(2):262-9. doi: 10.1016/s0163-1047(89)90902-3.
The effects of bilateral microinjections of chlordiazepoxide and GABA into the central amygdalar nucleus on gastric ulcer formation induced by cold-restraint were examined in chronically implanted Wistar rats. Higher doses of chlordiazepoxide (20 and 30 micrograms/amygdala) significantly reduced stress ulcer development, whereas a lower dose (2.5 micrograms) produced a nonsignificant increase in ulcer severity. A similar dose/response pattern was observed following GABA administration. The benzodiazepine receptor antagonist Ro15-1788, applied to the amygdala, abolished the protective effects of both chlordiazepoxide and GABA. In addition, when Ro15-1788 (10 micrograms) was injected into the amygdala by itself, it aggravated the gastric stress pathology. However, a lower dose (5 micrograms) had an attenuating effect, opposite to the pattern of effects produced by chlordiazepoxide and GABA. The role of the amygdalar GABA-benzodiazepine receptor complex in stressful conditions is discussed.
在长期植入的Wistar大鼠中，研究了向中央杏仁核双侧微量注射氯氮卓和GABA对冷束缚诱导的胃溃疡形成的影响。较高剂量的氯氮卓（20和30微克/杏仁核）显著减少了应激性溃疡的发展，而较低剂量（2.5微克）则使溃疡严重程度有不显著的增加。给予GABA后观察到类似的剂量/反应模式。应用于杏仁核的苯二氮卓受体拮抗剂Ro15 - 1788消除了氯氮卓和GABA的保护作用。此外，当单独将Ro15 - 1788（10微克）注入杏仁核时，它会加重胃应激病理。然而，较低剂量（5微克）具有减轻作用，这与氯氮卓和GABA产生的作用模式相反。讨论了杏仁核GABA - 苯二氮卓受体复合物在应激条件下的作用。
