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Interaction Between Nmda and Cb2 Function in the Dorsal Hippocampus on Memory Consolidation Impairment: An Isobologram Analysis Publisher Pubmed



Nasehi M1 ; Hajikhani M2 ; Ebrahimighiri M3 ; Zarrindast MR1, 4, 5, 6, 7, 8
Authors
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Authors Affiliations
  1. 1. Cognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences Branch, Islamic Azad University, P.O. Box 13145-784, Tehran, Iran
  2. 2. Department of Pharmacology and Toxicology, Islamic Azad University, Pharmaceutical Science Branch (IAUPS), Tehran, Iran
  3. 3. Department of Biology, Faculty of Sciences, University of Zanjan, Zanjan, Iran
  4. 4. Department of Pharmacology School of Medicine, Tehran University of Medical Sciences, P.O. Box 13145-784, Tehran, Iran
  5. 5. Institute for Cognitive Science Studies (ICSS), Tehran, Iran
  6. 6. Iranian National Center for Addiction Studies, Tehran University of Medical Sciences, Tehran, Iran
  7. 7. School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran
  8. 8. Medical Genomics Research Center, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran

Source: Psychopharmacology Published:2017


Abstract

Rationale: Convincing evidence has supported the pivotal role of N-methyl-d-aspartate receptors (NMDARs) and CB2Rs in the regulation of learning and memory. Objective: In this study, the role of hippocampal (CA1 region) CB2 receptors on aversive memory consolidation deficit induced by D-AP5, a NMDA receptor antagonist, was evaluated. Methods: Adult male Wistar rats received cannula implants that bilaterally targeted the CA1 region. Long-term memory was examined using the step-through type of passive avoidance task. Results: Post-training, intra-CA1 microinjection of D-AP5 (0.5 and 0.75 μg/rat), GP1a (CB2 receptor agonist at dose of 150 ng/rat) and AM630 (CB2 receptor antagonist at doses 75 and 100 ng/rat) impaired memory consolidation processes. Intra-CA1 microinjection of a lower dose of GP1a or AM630 restored memory impairment induced by D-AP5 at the two higher doses, while AM630 decreased D-AP5 memory response at the lower dose. The isobologram analysis showed that there is a synergistic effect between D-AP5 and AM630 on memory consolidation deficit. Conclusions: These results suggest that CA1 CB2 receptors modulate memory consolidation impairment induced by D-AP5. © 2016, Springer-Verlag Berlin Heidelberg.
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