Involvement of central amygdala muscarinic receptors in morphine-induced amnesia in rat

Learning and memory processes result from interaction of neurotransmitter systems in various brain regions such as amygdala and hippocampus. Considering that morphine induces memory impairment, in the current study, we examined the possible role of cholinergic muscarinic receptors of the central amygdala (CeA) on the morphine-induced amnesia in adult male Wistar rats. A week after the surgery during which cannulas were bilaterally implanted in the CeA nuclei of the amygdale, the animals were trained and tested in a step-through type passive avoidance task with 24 h interval time. Memory retrieval was measured by step-through latency, which is the latency to enter into the black shocked compartment. Post-training subcutaneous (s.c.) administration of morphine (5 and 7.5 mg/kg) dose-dependently decreased the step-through latency, suggesting morphine-induced amnesia. Post-training intra-CeA microinjection of pilocarpine (1 and 1.5 μg/rat), muscarinic receptor agonist, significantly decreased the amnesia induced by post-training administration of morphine (7.5 mg/kg s.c.). Moreover, post-training co-administration of a muscarinic receptor antagonist, scopolamine (0.5 and 0.6 μg/rat, intra-CeA) with an ineffective dose of morphine (2.5 mg/kg) inhibited memory retrieval. Post-training administration of the lower doses of scopolamine also reversed the influence of pilocarpine on the morphine response. It is important to note that post-training intra-CeA administration of the same doses of pilocarpine or scopolamine by itself had no effect on memory retrieval. The present results suggest that cholinergic muscarinic receptors of the central amygdala nuclei may play an important role in morphine-induced amnesia.