Open field habituation learning is improved by nicotine and attenuated by mecamylamine administered posttrial into the nucleus accumbens.

Using the paradigm of habituation learning in the open field, we tested the effects of unilateral microinjections of the agonist nicotine (8.0, 40.0, and 80.0 microg) and the nicotine receptor antagonist mecamylamine (0.1, 1.0, 10.0 microg) into the core of the nucleus accumbens. When injected posttrial, that is, immediately after the first exposure to the open field, nicotine dose-dependently enhanced behavioral habituation during the test on the following day, indicating a facilitation of memory, whereas mecamylamine impaired habituation at the highest dose, but not at the two lower doses. When injected 5 h after the learning trial, nicotine (40 microg) and mecamylamine (10 microg) impaired habituation on the subsequent day. A control experiment did not provide evidence for possible proactive effects of mecamylamine. These findings are discussed with respect to the possible behavioral functions of cholinergic, and especially nicotinic, mechanisms in the nucleus accumbens. They may also be relevant for understanding cholinergic-linked psychopathologies such as Alzheimer's disease, since the nucleus accumbens is one of the sites where cholinergic neurons are lost in this neurodegenerative disease. Copyright 2001 Elsevier Science (USA).