THE EFFECTS OF NICOTINE ADMINISTRATION ON PRO-OPIOMELANOCORTIN (POMC) AND µ OPIOID RECEPTOR (MOR) mRNA EXPRESSION IN THE RAT BRAIN
Project no. 60 · Status: Kapanmış · 2016
Summary
Pro-opiomelanocortin (POMC) is one of the important peptide precursors comprising the endogenous opioidergic system. POMC-derived peptides have a role in processes such as stress response, feeding behavior and drug abuse. ß-endorphin, a neuropeptide synthesized from POMC, plays a key role in addiction. The aim of our study was to investigate the regulatory actions of nicotine on POMC and the ß-endorphin-binding µ-opioid receptor (MOR) mRNAs in the anatomical structures that constitute the mesocorticolimbic system, which is recognized for its central role in the motivation and reward-related behavior. Accordingly, one of three doses of nicotine (0.2, 0.4, 0.6 mg/kg and saline) was injected into the rats for five days and rats were decapitated one hour after the last injection on the sixth day of treatment. POMC mRNA expression in the medial hypothalamic area (MHA) (arcuate nucleus) and MOR mRNA expression in the medial prefrontal cortex (mPFC), nucleus accumbens (NAc), dorsal striatum (DST), amygdala (AMG), lateral hypothalamic area (LHA) and ventral tegmental area (VTA) were evaluated by using quantitative real-time PCR method. Our results showed that POMC mRNA levels in the hypothalamus were upregulated in rats, which received 0.6 mg/kg nicotine. However, none of the nicotine doses altered MOR mRNA levels in the mesocorticolimbic regions and the associated limbic structures. These results suggest that nicotine may increase POMC signaling in the mesocorticolimbic system and that this change may be an important mechanism in mediating the nicotine reward.