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Involvement of Medial Prefrontal Cortex Alpha-2 Adrenoceptors on Memory Acquisition Deficit Induced by Arachidonylcyclopropylamide, a Cannabinoid Cb1 Receptor Agonist, in Rats; Possible Involvement of Ca2+ Channels Publisher Pubmed



Beiranvand A1 ; Nasehi M2 ; Zarrindast MR1, 2, 3, 4, 5 ; Moghaddasi M6
Authors

Source: Journal of Psychopharmacology Published:2016


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. © British Association for Psychopharmacology.
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