Effects of cadmium on memory processes in mice exposed to transient cerebral oligemia

Abstract

The purpose of the present study was to examine whether the effects of chronic or acute exposure to cadmium on memory processes in mice could be exacerbated by transiently reducing cerebral oxygen supply. Adult mice were subjected to bilateral clamping of the carotid artery (BCCA) for 30 min under anesthesia. Cadmium chloride was administered intraperitoneally after surgery at single doses of: 0.7 mg/kg (low dose), 1.4 mg/kg (high dose), or at a prolonged dose of 0.7 mg/kg for up to 10 days. Long-term memory was evaluated in a step-through passive avoidance task while spatial working memory was evaluated using a Y-maze spontaneous alternation task. BCCA mice injected with the 1.4 mg/kg dose of cadmium exhibited recall deficits in the step-through passive avoidance task. Combined treatment at either dose had no effect on the acquisition of passive avoidance. In the Y-maze task, spontaneous alternation behavior was only impaired in BCCA mice treated with the prolonged cadmium dose. These results indicate that cerebral oligemic hypoxia may alter cadmium neurotoxicity and potentiate the tendency for cadmium-induced memory impairments in the passive avoidance task and spontaneous alternation deficits.