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Possible Involvement of the Ca1 Gabaa Receptors Upon Acquisition and Expression of the Acpa-Induced Place Preference in Mice Publisher Pubmed



Nasehi M1 ; Kamalidolatabadi L2, 3 ; Torabinami M2, 4 ; Zarrindast MR1, 5, 6, 7, 8, 9, 10
Authors
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Authors Affiliations
  1. 1. Cognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran
  2. 2. Department of Neuroscience, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran
  3. 3. Department of Biology, Faculty of Basic Sciences, Islamic Azad University, Northern Branch, Tehran, Iran
  4. 4. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
  5. 5. Iranian National Center for Addiction Studies, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran
  7. 7. Institute for Cognitive Science Studies (ICSS), Tehran, Iran
  8. 8. Department of Pharmacology School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  9. 9. Medical Genomics Research Center, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran
  10. 10. Department of Pharmacology School of Medicine, Tehran University of Medical Sciences, P.O. Box 13145-784, Tehran, Iran

Source: Physiology and Behavior Published:2016


Abstract

A plethora of investigations has substantiated a close relationship between cannabinoidergic and GABAergic systems in hippocampal CA1. The crucial role of these two systems in regulation of the addictive behaviors is well described. The aim of the current study was to investigate whether the CA1 GABAA receptors are involved in ACPA (a selective CB1 cannabinoid receptor agonist)-induced rewarding effects using the condition place preference (CPP) protocol. Moreover, the hole-board paradigm was used to measure the exploratory behaviors which may potentially influence this phenomenon. Results showed that ACPA (0.02 mg/kg, i.p.) induced CPP. Applying a 3-day conditioning schedule, we found that the sole administration of the GABAA receptor agonist, muscimol (0.125, 0.25 and 0.5 μg/mouse; intra-CA1), or the GABAA receptor antagonist, bicuculline (0.0635, 0.125 and 0.25 μg/mouse; intra-CA1), fail to induce CPP or CPA (condition place aversion). Similarly, injection of the subthreshold dose of muscimol (0.125 μg/mouse, intra-CA1) decreased the CPP acquisition induced by ACPA. Similar intervention with the subthreshold dose of bicuculline (0.125 μg/mouse, intra-CA1) did not alter the CPP acquisition induced by ACPA. Furthermore, the sole intra-CA1 administration of muscimol (0.125, 0.25 and 0.5 μg/mouse) and bicuculline (0.0635, 0.125 and 0.25 μg/mouse; intra-CA1) prior to testing, did not induce CPP or CPA. Similar interventions revealed that muscimol and bicuculline increase and decrease CPP expression induced by ACPA, respectively. The ACPA- and muscimol-induced CPP could be blocked by bicuculline. Taken together, the CA1 GABAA receptors seem to be possibly involved in the modulation of acquisition or expression process upon ACPA-induced CPP. © 2016 .
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