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“School of Cognitive Sciences”

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Paper   IPM / Cognitive Sciences / 11299
School of Cognitive Sciences
  Title:   Nicotine improves ethanol-induced memory impairment: The role of dorsal hippocampal NMDA receptors
1.  Ameneh Rezayof
2.  Zahra Shirazi-Zand
3.  Mohammad Reza Zarrindast
4.  Touraj Nayer-Nouri
  Status:   Published
  Journal: Life Sciences
  Vol.:  86
  Year:  2010
  Pages:   260-266
  Supported by:  IPM
Aims: The current study was undertaken to determine the role of dorsal hippocampal N-methyl-D-aspartate (NMDA) receptors in nicotine's effect on impairment of memory by ethanol. Main methods: Adult male mice were cannulated in the CA1 regions of dorsal hippocampi and trained on a passive avoidance learning task for memory assessment. Key findings: We found that pre-training intraperitoneal (i.p.) administration of ethanol (0.5 and 1 g/kg) decreased memory retrieval when tested 24 h later. Pre-test administration of ethanol reversed the decrease in inhibitory avoidance response induced by pre-training ethanol. Similar to ethanol, pre-test administration of nicotine (0.125?0.75 mg/kg, s.c.) prevented impairment of memory by pre-training ethanol. In the animals that received ethanol (1 g/kg, i.p) before training and tested following intra-CA1 administration of different doses of NMDA (0.0005?0.005 μg/mouse), no significant change was observed in the retrieval latencies. Coadministration of the same doses of NMDA with an ineffective dose of nicotine (0.125 mg/kg, s.c.) significantly improved the memory retrieval and mimicked the effects of pre-test administration of a higher dose of nicotine. Pre-test intra-CA1 microinjection of MK-801 (0.25?1 μg/mouse), which had no effect alone, in combination with an effective dose of nicotine (0.75 mg/kg, s.c.) prevented the improving effect of nicotine on memory impaired by pre-training ethanol. Moreover, intra-CA1 microinjection of MK-801 reversed the NMDA-induced potentiation of the nicotine response. Significance: The results suggest the importance of NMDA glutamate system(s) in the CA1 regions of dorsal hippocampus for improving the effect of nicotine on the ethanol-induced amnesia.

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