Yadin E, Thomas E, Strickland C E, Grishkat H L
Department of Psychology, Bryn Mawr College, Pennsylvania, PA 19010.
Psychopharmacology (Berl). 1991;103(4):473-9. doi: 10.1007/BF02244247.
The role of the amygdala in the anxiolytic action of benzodiazepines was examined. Performance on a water-licking conflict paradigm was tested in rats with localized damage to the central nucleus of the amygdala (ACE) or with general damage to the entire amygdaloid complex. The effects of the benzodiazepine chlordiazepoxide (2.5-20.0 mg/kg) on conflict behavior in these animals was also examined. Electrolytic lesions of either ACE or of the entire amygdaloid complex resulted in a pronounced increase of punished responding, an effect that persisted for at least 12 sessions postoperatively. After shock levels were adjusted in the lesioned groups to match their baseline punished behavior to that of the controls, various doses of chlordiazepoxide were administered. Not only did the lesioned animals show an increase in punished behavior in response to the drug, they were more sensitive than controls to the lower drug doses. A complete model of anxiolytic action may have to include both mechanisms that block anxiogenic regions and those that activate anxiolytic regions.
研究了杏仁核在苯二氮䓬类抗焦虑作用中的角色。在杏仁核中央核局部损伤（ACE）或整个杏仁复合体广泛损伤的大鼠中，测试其在舔水冲突范式中的行为表现。还研究了苯二氮䓬类药物氯氮䓬（2.5 - 20.0毫克/千克）对这些动物冲突行为的影响。ACE或整个杏仁复合体的电解损伤导致受惩罚反应显著增加，这种效应在术后至少12个实验阶段持续存在。在损伤组中调整电击水平，使其基线受惩罚行为与对照组相匹配后，给予不同剂量的氯氮䓬。损伤动物不仅对药物反应表现出受惩罚行为增加，而且比对照组对较低药物剂量更敏感。完整的抗焦虑作用模型可能必须包括阻断致焦虑区域的机制和激活抗焦虑区域的机制。
