Abstract

The purpose of the present investigation was to the potential role of acetylcholine(Ach) in escape interference in rats produced by inescapable shock. The centrally acting anticholinergic, scopolamine hydrobromide(1.0mg/kg) eliminated the disruptive effects of previously adminstered inescapable shock. In contrast, the anticholinestrase, physostimine salicylate (0.1mg/kg) successfully mimicked the effects of inescapable shock. The escape interference effect of inescapable shock was facilitated by treament with physostigmine(Exp.1). The elimination of the escape deficits by scopolamine administration might not be a result of asymmetrical state dependence(Exp.2). The centrally acting scopolamine substantially antagonized the effecsts of physostigmine(Exp.3). It was concluded that inescapable shock is involved in central Ach changes. This result supported the "Ach hypothesis" in the explanation of the escape deficits of the rats following uncontrollable stress. It was speculatively argued that inescapable shock might activate septo-hippocampal behavioral inhibition system, which is mediated by an increase in Ach activity.