cortex alpha-2 adrenoceptors on memory acquisition deficit induced by arachidonylcyclopropylamide, a cannabinoid CB1 receptor agonist, in rats; possible involvement of Ca2+ channels

Beiranvand, Afsaneh and Nasehi, Mohammad and Zarrindast, Mohammad-Reza and Moghaddasi Jahromi, Mehrnoush (2016) cortex alpha-2 adrenoceptors on memory acquisition deficit induced by arachidonylcyclopropylamide, a cannabinoid CB1 receptor agonist, in rats; possible involvement of Ca2+ channels. Journal of Psychopharmacology.

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Abstract

Functional interactions between cannabinoid and alpha-2 adrenergic systems in cognitive control in the medial prefrontal cortex (mPFC) seem possible. The present study evaluated the possible role of alpha-2 adrenoceptors of the prefrontal cortex on effect of arachidonylcyclopropylamide (ACPA), a cannabinoid CB1 receptor (CB1R) agonist, in adult male Wistar rats. The animals were bilaterally implanted with chronic cannulae in the mPFC, trained in a step-through task, and tested 24 h after training to measure step-through latency. Results indicate that pre-training microinjection of ACPA (0.05 and 0.5 μg/rat) and clonidine (alpha-2 adrenoceptor agonist; 1 and 2 μg/rat) reduce memory acquisition. Pre-training subthreshold dose of clonidine (0.5 μg/rat) restored memory-impairing effect of ACPA (0.05 and 0.5 μg/rat). On the other hand, pre-training administration of the alpha-2 adrenoceptor antagonist yohimbine in all doses used (0.5, 1, and 2 μg/rat) did not affect memory acquisition by itself, while a subthreshold dose of yohimbine (2 μg/rat) potentiated memory impairment induced by ACPA (0.005 μg/rat). Finally, a subthreshold dose of SKF96365 (a Ca2+ channel blocker) blocked clonidine and yohimbine effect of memory responses induced by ACPA. In conclusion, these data indicate that mPFC alpha-2 adrenoceptors play an important role in ACPA-induced amnesia and Ca2+ channels have a critical role this phenomenon.

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