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| Paper IPM / Cognitive / 8965 |
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| Abstract: | |||||||||
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In the present study, the effects of bilateral injections of cholinergic agents into
the hippocampal CA1 regions (intra-CA1) on ethanol state-dependent memory
were examined in mice. A single-trial step-down passive avoidance task was used
for the assessment of memory retention in adult male NMRI mice. Pre-training
intraperitoneal injection (i.p.) of ethanol (0.25, 0.5 and 1 g/kg) dose dependently
induced impairment of memory retention. Pre-test administration of ethanol (0.5
and 1 g/kg, i.p.) induced state-dependent retrieval of the memory acquired under
pre-training ethanol (1 g/kg, i.p.) influence. Pre-test intra-CA1 injection of
physostigmine (2.5 and 5 lg/mouse, intra-CA1) or nicotine (0.3 and 0.5 lg/mouse,
intra-CA1) improved pre-training ethanol (1 g/kg)-induced retrieval impairment.
Moreover, pre-test administration of physostigmine (2.5 and 5 lg/mouse, intra-
CA1) or nicotine (0.3 and 0.5 lg/mouse, intra- CA1) with an ineffective dose of
ethanol (0.25 g/kg) significantly restored the retrieval and induced ethanol statedependent
memory. Pre-test intra-CA1 injection of the muscarinic receptor
antagonist, atropine (4 and 8 lg/mouse, intra-CA1) or the nicotinic receptor
antagonist, mecamylamine (2 and 4 lg/mouse, intra-CA1) 5 min before the
administration of ethanol (1 g/kg, i.p.) dose dependently inhibited ethanol statedependent
memory. Pre-test intra-CA1 administration of physostigmine (0.5, 2.5
and 5 lg/mouse), atropine (2, 4 and 8 lg/mouse), nicotine (0.1, 0.3 and 0.5
lg/mouse) or mecamylamine (1, 2 and 4 lg/mouse) alone cannot affect memory
retention. These findings implicate the involvement of a dorsal hippocampal
cholinergic mechanism in ethanol state-dependent memory and also it can be
concluded that there may be a cross-state dependency between ethanol and
acetylcholine.
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