The effects of nicotine administration on the mch and mchr1 expression in the rat brain

Melanin concentrating hormone (MCH) and its receptor MCHR1 show intense expression in the mesocorticolimbic pathway, which is referred to as the reward system. It has been suggested that MCH signaling may play a role in the rewarding effects of addictive agents such as alcohol, cocaine, amphetamine, methamphetamine as well as natural substances such as sucrose and food. The aim of our study is to investigate the regulation of MCH and MCHR1 mRNA in anatomic structures which compose the mesocorticolimbic system, during the emergence of rewarding effect of nicotine. For this purpose, adult male rats were subcutaneously injected with three different doses of nicotine (0.2, 0.4, 0.6 mg/kg or saline) for six days; decapitation was performed one hour after the last injection. MCH mRNA expression in the lateral hypothalamic area (LHA) and MCHR1 mRNA expression in the amygdala (AMG), medial prefrontal cortex (mPFC), nucleus accumbens (NAc), dorsal striatum (DST), lateral hypothalamic area (LHA), medial hypothalamic area (MHA) and ventral tegmental area (VTA) were analyzed by using quantitative real-time PCR (qPCR) method. Our results showed that none of the administered nicotine doses altered MCH and MCHR1 mRNA expression in the examined brain regions. These results suggest that MCH signaling is not regulated in the mesocorticolimbic system during nicotine reward. Key words: nicotine; MCH; MCHR1; mesocorticolimbic system