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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
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Authors Affiliations
  1. 1. Institute for Cognitive Science Studies (ICSS), Tehran, Iran
  2. 2. Cognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences Branch, Islamic Azad University, P.O. Box 13145-784, Tehran, Iran
  3. 3. Iranian National Center for Addiction Studies, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran
  5. 5. Razi Herbal Medicines Research Center, Department of Physiology, Lorestan University of Medical Sciences, Khorramabad, Iran
  6. 6. Medical Genomics Research Center, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran

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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