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چکیده
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In the present study, we investigated effects of intra-central amygdala (intra-CeA) administrations of a β1- receptor agonist and antagonist, isoprenaline (isoproterenol) and atenolol respectively, on state-dependent memory induced by a cannabioid agonist, WIN55,212-2. This study used a step-through inhibitory avoidance task to assess memory in male Wistar rats. The results showed that post-training intra-CeA administrations of different doses of WIN55,212-2 (0.01, 0.05, 0.1 and 0.25 µg/rat) decreased memory as revealed by a decrease in memory retrieval on the test day. The decrease in retrieval induced by post-training WIN55, 212-2 (0.25 µg/rat) was reversed by pre-test administration of the same dose of the drug, which was suggestive of drug-induced state-dependent memory. Although pre-test intra-CeA administrations of isoprenaline (0.01, 0.025 and 0.05 µg/rat) alone had no effect, its co-administrations at doses of 0.025 and 0.05 µg/rat with an ineffective dose of WIN55, 212-2 (0.1 µg/rat) restored memory retrieval that impaired by post-training WIN55, 212-2 (0.25 µg/rat). The results also showed that pre-test intra-CeA administrations of atenolol (0.01, 0.05 and 0.1 µg/rat) alone had no effect, but at dose of 0.1 µg/rat disrupted state-dependent memory induced by WIN55, 212-2. Moreover, the improving effect of isoprenaline (0.025 µg/rat) on retrieval of state-dependent memory induced by WIN55, 212-2 (0.1 µg/rat) was prevented by intra-CeA co-injections of atenolol. Taken together, our results suggest that the CeA may be potentially critical for state-dependent memory induced by WIN55, 212-2 and the β1-noradrenergic receptor mechanism(s) interact with the cannabinergic system in the modulation of this kind of memory in the CeA.
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