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| Paper IPM / Cognitive / 11299 |
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| Abstract: | |||||||||
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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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