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The present study investigated the possible involvement of the central amygdala (CeA) cannabinoid receptors type-1 (CB1Rs) in the interactive effects of morphine and nicotine on memory formation in a passive avoidance learning task. Our results showed that systemic administration of morphine (3 and 6 mg/kg, s.c.) immediately after training phase impaired memory consolidation and induced amnesia. Administration of nicotine (0.3 and 0.6 mg/kg, s.c.) before testing phase significantly restored morphine-induced amnesia, suggesting a cross state-dependent learning between morphine and nicotine. The results showed that while the administration of the lower dose of nicotine (0.1 mg/kg, s.c.) per se did not induce a significant effect on morphine-induced amnesia, intra-CeA injection of arachidonylcyclopropylamide (ACPA), a cannabinoid CB1 receptor agonist (3 and 4 ng/rat), significantly potentiated the nicotine response. Furthermore, the blockade of the CeA cannabinoid CB1 receptors by the injection of AM251 (0.75 and 1 ng/rat) reversed the potentiative effect of nicotine (0.6 mg/kg, s.c.) on morphine-induced amnesia. It should be considered that bilateral injection of the same doses of ACPA or AM251 (0.5–1 ng/rat) into the CeA by itself had no effect on morphine response in a passive avoidance learning task. Confirmed by the cubic interpolation planes, the dose-response data revealed a cross-state-dependent learning between morphine and nicotine which may be mediated by the CeA endocannabinoid system via CB1 receptors.Morphine administration induced amnesia.Nicotine reversed morphine response, suggesting a cross state-dependent learning.Intra-CeA injection of ACPA potentiated morphine/nicotine response.Intra-CeA injection of AM251 reversed nicotine response on morphine amnesia.