CHRONIC NICOTINE ENHANCES BASAL AND NICOTINE-INDUCED FOS IMMUNOREACTIVITY PREFERENTIALLY IN THE MEDIAL PREFRONTAL CORTEX OF THE RAT

In the present study, expression of the immediate early gene protein p roducts Fos and Jun-B within the dorsolateral striatum, the core and s hell of the nucleus accumbens (NAG), the medial prefrontal cortex (mPF C), and the ventrolateral orbital col tex was examined. Rats were inje cted SC with either saline or nicotine (0.5 mg/kg) once daily for 12 d ays. On day 13, animals received a challenge injection of either salin e or nicotine (0.5 or 1.0 mg/kg, SC) and 2 h later their brains were e xamined for Fos-like (FLI) and Jun-B-like (JLI) immunoreactivity. Chro nic nicotine significantly increased basal expression of FLI selective ly in the mPFC. Nicotine challenge significantly increased FLI in the mPFC of saline-treated animals and even further increased FLI in the m PFC of nicotine-treated animals. In the shell of the NAG, nicotine cha llenge also increased FLI in nicotine-treated animals, whereas if incr eased JLI only in saline-treated animals. After chronic nicotine treat ment, injection of D-1 receptor antagonist SCH 23390 (0.1 mg/kg, IP) 1 0 min before a nicotine challenge (0.5 mg/kg, SC), significantly atten uated the nicotine-induced FLI in the mPFC and the shell of the NAG. T hese results suggest that the regionally selective effect of nicotine challenge on FLI is due to enhanced dopaminergic transmission, mediate d via stimulation of D-1 receptors. (C) 1997 American College of Neuro psychopharmacology. Published by Elsevier Science Inc.