Ethanol state-dependent memory: Involvement of dorsal hippocampal muscarinic and nicotinic receptors

In the present study, the effects of bilateral injections of cholinergic agents into the hippocampal CAI regions (intra-CAI) 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 I g/kg, i.p.) induced state-dependent retrieval of the memory acquired under pre-training ethanol (I g/kg, i.p.) influence. Pre-test intra-CAI injection of physostigmine (2.5 and 5 mu g/mouse, intra-CAI) or nicotine (0.3 and 0.5 mu g/mouse, intra-CAI) improved pre-training ethanol (1 g/kg)-induced retrieval impairment. Moreover, pre-test administration of physostigmine (2.5 and 5 mu g/mouse, intra-CAI) or nicotine (0.3 and 0.5 mu g/mouse, intra-CAI) with an ineffective dose of ethanol (0.25 g/kg) significantly restored the retrieval and induced ethanol state-dependent memory. Pre-test intra-CAI injection of the muscarinic receptor antagonist, atropine (4 and 8 mu g/mouse, intra-CAI) or the nicotinic receptor antagonist, mecamylamine (2 and 4 mu g/mouse, intra-CAI) 5 min before the administration of ethanol (I g/kg, i.p.) dose dependently inhibited ethanol state-dependent memory. Pre-test intra-CAI administration of physostigmine (0.5, 2.5 and 5 mu g/mouse), atropine (2, 4 and 8 mu g/mouse), nicotine (0.1, 0.3 and 0.5 mu g/mouse) or mecamylamine (1, 2 and 4 pg/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. (C) 2007 Elsevier Inc. All rights reserved.