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Role of Ca1 Gabaa and Gabab Receptors on Learning Deficit Induced by D-Ap5 in Passive Avoidance Step-Through Task Publisher Pubmed



Ebrahimighiri M1 ; Rostampour M2 ; Jamshidimehr M3 ; Nasehi M4 ; Zarrindast MR2, 5, 6, 7, 8, 9
Authors
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Authors Affiliations
  1. 1. Department of Biology, Faculty of Sciences, University of Zanjan, Zanjan, Iran
  2. 2. Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Department of Physiology, Shiraz University of Medical Sciences, Shiraz, Iran
  4. 4. Cognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences Branch, Islamic Azad University, Tehran, 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. Medical Genomics Research Center, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran
  8. 8. Institute for Cognitive Science Studies (ICSS), Tehran, Iran
  9. 9. University of Social Welfare and Rehabilitation Sciences, Tehran, Iran

Source: Brain Research Published:2018


Abstract

To investigate the interaction between hippocampal γ-aminobutyric acid GABAA receptor (GABAAR) or GABAB receptor (GABABR) and N-methyl-D-aspartate receptor (NMDAR) in the acquisition of passive avoidance memory in rats, we used GABAA or GABAB agents, D-AP5 (as a NMDAR antagonist), and a combination of the mentioned drugs in a step-through task. All agents were microinjected into the intra-CA1 regions at a volume of 1 µl/rat, prior to training. GABAAR agonist muscimol (0.2 µg/rat), selective GABABR agonist baclofen (0.5 µg/rat) or NMDAR antagonist D-AP5 (0.25 µg/rat) decreased step-through latency, indicating a memory retention impairment. Neither GABAAR antagonist bicuculline (0.0625–0.25 µg/rat) nor GABABR antagonist phaclofen (0.1–0.5 µg/rat) altered memory retrieval by itself. Moreover, the lower dose of muscimol (0.05 µg/rat) decreased D-AP5 (0.125 µg/rat) response on memory acquisition, but bicuculline did not alter the D-AP5 response. Furthermore, baclofen and phaclofen at the dose of 0.1 µg/rat potentiated D-AP5 response at the doses of 0.0625 and 0.125 µg/rat, but abolished memory impairment induced by D-AP5 at the higher dose (0.25 µg/rat). The results suggest that the microinjection of GABAA and GABAB agents into the CA1 region differently affects memory acquisition deficit induced by D-AP5. The activation of GABAARs increased the impairment effect of D-AP5 on passive avoidance memory, but their blockade did not have an effect. Also, the activation or blockade of GABABRs induced a similar and dual effect. © 2017
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