Effect of acute nicotine on Fos protein expression in rat brain during chronic nicotine and its withdrawal

To study the cholinergic regulation of hypothalamic paraventricular (PVN) a nd supraoptic (SON) nuclei and interpeduncular nucleus (IPN) we investigate d the effects of acute nicotine (0.5 mg/kg, SC, 60 min) on Fos-like immunos taining (IS) during chronic nicotine and its withdrawal in rats. Nicotine o r saline was infused to rats via osmotic minipumps (4 mg/kg/day) for 7 days ; on the seventh day, the minipumps were removed surgically. In control rat s, acute nicotine increased Fos IS significantly in all three brain areas s tudied. On the seventh day of nicotine infusion this effect partially persi sted in IPN but was abolished in PVN and SON. After 72-h withdrawal nicotin e-induced elevation of Fos IS was similar to that of control rats in all th ree areas. The observed attenuation of the response to acute nicotine durin g constant nicotine infusion in PVN and SON may be attributable to the dese nsitization of nicotinic acetylcholine receptors (nAChRs) mediating the eff ects of nicotine in these areas or in their input areas. IPN is connected t o midbrain limbic system, so in agreement with our earlier observations, it seems that limbic nicotinic receptors do not very readily desensitize duri ng chronic nicotine infusion. These findings support the suggestions that t here are differences in the level of desensitization of nAChRs. (C) 2000 El sevier Science Inc.