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IPM
30
YEARS OLD

“School of Cognitive Sciences”

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Paper   IPM / Cognitive Sciences / 13207
School of Cognitive Sciences
  Title:   Interaction between gamma-aminobutyric acid type A (GABAA) receptor agents and scopolamine in the nucleus accumbens on impairment of inhibitory avoidance memory performance in rat
  Author(s): 
1.  R. Azizbeigi
2.  M.R. Zarrindast
3.  S. Ahmadi
  Status:   Published
  Journal: Behavioural Brain Research
  Vol.:  241
  Year:  2013
  Pages:   191-197
  Supported by:  IPM
  Abstract:
We designed this study to investigate effects of intra-nucleus accumbens (intra-NAc) infusions of GABAA receptors agonist (muscimol) and antagonist (bicuculline) by themselves and their interaction with scopolamine on inhibitory avoidance (IA) memory performance. This study used a step-through IA task to assess memory in male Wistar rats. The results showed that post-training intra-NAc infusions of muscimol at doses of 0.01 and 0.02 g/rat significantly impaired IA memory performance, while bicuculline (0.1, 0.2 and 0.4 g/rat) had no effect. Post-training intra-NAc infusions of scopolamine at dose of 0.5 g/rat impaired IA memory performance by itself, and in combination with an ineffective dose of muscimol increased impairment of IA memory performance. The results also showed that post-training intra-NAc infusions of bicuculline prevented the impairing effect of higher doses of scopolamine on IA memory performance. Pre-test intra-NAc infusions of muscimol (0.01 and 0.02 g/rat) and bicuculline (0.001, 0.01 and 0.1 g/rat) impaired IA memory performance. The results also revealed that pre-test intra-NAc infusions of scopolamine (0.25 and 0.5 g/rat) impaired IA memory performance, and its co-infusions with an ineffective dose of muscimol (0.005 g/rat) increased impairment of IA memory performance. Interestingly, pre-test intra-NAc infusions of bicuculline impaired performance by itself, but did not prevent the impairing effect of scopolamine. It can be concluded that GABAA and muscarinic receptors of the NAc may have an interaction in modulation of IA memory performance, which may result from affecting output neurons in the NAc directly or indirectly via cholinergic and GABAergic interneurons.

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