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 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 1g/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 microg/mouse, intra-CA1) or nicotine (0.3 and 0.5 microg/mouse, intra-CA1) improved pre-training ethanol (1g/kg)-induced retrieval impairment. Moreover, pre-test administration of physostigmine (2.5 and 5 microg/mouse, intra-CA1) or nicotine (0.3 and 0.5 microg/mouse, intra-CA1) with an ineffective dose of ethanol (0.25 g/kg) significantly restored the retrieval and induced ethanol state-dependent memory. Pre-test intra-CA1 injection of the muscarinic receptor antagonist, atropine (4 and 8 microg/mouse, intra-CA1) or the nicotinic receptor antagonist, mecamylamine (2 and 4 microg/mouse, intra-CA1) 5 min before the administration of ethanol (1g/kg, i.p.) dose dependently inhibited ethanol state-dependent memory. Pre-test intra-CA1 administration of physostigmine (0.5, 2.5 and 5 microg/mouse), atropine (2, 4 and 8 microg/mouse), nicotine (0.1, 0.3 and 0.5 microg/mouse) or mecamylamine (1, 2 and 4 microg/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.
Rezayof
Ameneh
A
Department of Animal Biology, School of Biology, College of Science, University of Tehran, P.O. Box 14155-6455, Tehran, Iran. rezayof@khayam.ut.ac.ir
Alijanpour
Sakineh
S
Zarrindast
Mohammad-Reza
MR
Rassouli
Yassaman
Y
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001362:Avoidance Learning / Q000187:drug effects / Q000502:physiology; D002492:Central Nervous System Depressants / Q000494:pharmacology*; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D000431:Ethanol / Q000494:pharmacology*; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology; D008297:Male; D008464:Mecamylamine / Q000494:pharmacology; D008568:Memory / Q000187:drug effects* / Q000502:physiology; D051379:Mice; D008815:Mice, Inbred Strains; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009538:Nicotine / Q000494:pharmacology; D018722:Nicotinic Agonists / Q000494:pharmacology; D018733:Nicotinic Antagonists / Q000494:pharmacology; D010830:Physostigmine / Q000494:pharmacology; D011976:Receptors, Muscarinic / Q000502:physiology*; D011978:Receptors, Nicotinic / Q000502:physiology*
D002492:Central Nervous System Depressants; D002800:Cholinesterase Inhibitors; D018727:Muscarinic Antagonists; D018722:Nicotinic Agonists; D018733:Nicotinic Antagonists; D011976:Receptors, Muscarinic; D011978:Receptors, Nicotinic; D000431:Ethanol; D008464:Mecamylamine; D009538:Nicotine; D001285:Atropine; D010830:Physostigmine