Exercise abolishes the rewarding (dopamine) aspects of drugs (2008)
COMMENTS: Ecstasy using rats have a spike in dopamine and develop what's called conditioned place preference- which is preferring to hang out in the place where they experienced an unusually strong reward. Rats & people with addictions experience conditioned place preference. In fact, returning to the place of former drug use is a huge trigger for relapse.
In this study aerobic exercise (wheel running) abolished the dopamine spike normally caused by Ecstasy, and the conditioned place preference. In essence it abolished any hints of an addiction. It did so without negatively affecting dopamine and dopamine receptors. Remember that all addictions share common mechanisms and brain pathways, especially dopamine dysregulation. So exercise.
Behav Brain Res. 2008 Feb 11;187(1):185-9. Epub 2007 Sep 16.
Chen HI, Kuo YM, Liao CH, Jen CJ, Huang AM, Cherng CG, Su SW, Yu L.
Department of Physiology, National Cheng Kung University College of Medicine, Tainan 701, Taiwan, ROC.
Although exercise has been known to regulate brain plasticity, its impact on psychostimulant reward and the associated mesolimbic dopamine system remained scarcely explored. A psychostimulant, 3,4-methylenedioxymethamphetamine (MDMA), is currently a worldwide abused drug of choice. We decided to examine the modulating effects of long-term, compulsive treadmill exercise on the hedonic value of MDMA in male C57BL/6J mice.
MDMA-induced conditioned place preference (CPP) was used as a behavioral paradigm to indicate the reward efficacy of MDMA. We observed that sedentary control mice all demonstrated reliable MDMA-induced CPP with our conditioning protocol. Interestingly, pre-exposure to a treadmill exercise decreased the later MDMA-induced CPP in a running period-dependent manner. Specifically, mice undergoing a 12-week treadmill running exercise did not exhibit any approaching bias toward the MDMA-associated compartment in this CPP paradigm.
Twelve weeks of treadmill running did not alter peripheral metabolism of MDMA 30min following single intraperitoneal injection of MDMA (3mg/kg). We further used microdialysis technique to study the underlying mechanisms for the impaired MDMA reward produced by the 12-week exercise pre-exposure. We found that acute MDMA-stimulated dopamine release in nucleus accumbens was abolished in the exercised mice, whereas an obvious elevation of accumbal dopamine release was observed in sedentary control mice.
Finally, the 12-week exercise program did not alter the protein levels of primary dopamine receptors, vesicular or membrane transporters in this area. We conclude that the long-term, compulsive exercise is effective in curbing the reward efficacy of MDMA possibly via its direct effect on reversing the MDMA-stimulated dopamine release in nucleus accumbens.