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| Paper IPM / Cognitive Sciences / 15921 |
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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 1â¯Âµl/rat, prior to training. GABAAR agonist muscimol (0.2â¯Âµg/rat), selective GABABR agonist baclofen (0.5â¯Âµg/rat) or NMDAR antagonist D-AP5 (0.25â¯Âµg/rat) decreased step-through latency, indicating a memory retention impairment. Neither GABAAR antagonist bicuculline (0.0625-0.25â¯Âµg/rat) nor GABABR antagonist phaclofen (0.1-0.5â¯Âµg/rat) altered memory retrieval by itself. Moreover, the lower dose of muscimol (0.05â¯Âµg/rat) decreased D-AP5 (0.125â¯Âµg/rat) response on memory acquisition, but bicuculline did not alter the D-AP5 response. Furthermore, baclofen and phaclofen at the dose of 0.1â¯Âµg/rat potentiated D-AP5 response at the doses of 0.0625 and 0.125â¯Âµg/rat, but abolished memory impairment induced by D-AP5 at the higher dose (0.25â¯Âµg/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.
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