The epigenetic effect of nicotine on dopamine D1 receptor expression in rat prefrontal cortex.

摘要: Nicotine is a highly addictive drug and exerts its effect partially through causing dopamine release, thereby increasing intrasynaptic levels in the brain reward systems. Dopaine D1 receptor (DRD1) mRNAs receptors are localized reward-related regions, which receive cholinergic input. The aim of this study to evaluate whether nicotine administration affects expression DRD1s, if so, epigenetic mechanisms, such as histone acetylation, involved. Twenty Male Sprague Dawley rats received (0.4 mg/kg/day, s.c.) or saline injections for 15 days. After nicotine/saline treatment, were perfused with saline; prefrontal cortex (PFC), corpus striatum (STR), ventral tegmental area (VTA) dissected. Homogenates divided into two parts total RNA isolation H4 acetylation studies. DRD1 mRNA was significantly higher PFC nicotine-treated group compared controls; similar trends observed VTA STR. To regulation, 2kb upstream region gene promoter investigated samples. chromatin immunoprecipitation anti-acetyl antibody, we found an increase by different primer pairs amplified −1365 −1202 (P < 0.005) −170 +12 (P < 0.05) regions promoter. Our results suggest that intermittent subcutaneous increases rats, may be due changes gene. Synapse 67:545–552, 2013. © 2013 Wiley Periodicals, Inc.