Dopamine in the Brain: Hypothesizing Surfeit or Deficit Links to Reward and Addiction

Kenneth Blum, Peter K. Thanos, Marlene Oscar-Berman, Marcelo Febo, David Baron, Rajendra D. Badgaiyan, Eliot Gardner, Zsolt Demetrovics, Claudia Fahlke, Brett C. Haberstick, Kristina Dushaj and Mark S. Gold



Recently there has been debate concerning the role of brain dopamine in reward and addiction. David Nutt and associates eloquently proposed that dopamine (DA) may be central to psycho stimulant dependence and some what important for alcohol, but not important for opiates, nicotine or even cannabis. Others have also argued that surfeit theories can explain for example cocaine seeking behavior as well as non-substance-related addictive behaviors. It seems prudent to distinguish between what constitutes “surfeit” compared to” deficit” in terms of short-term (acute) and long-term (chronic) brain reward circuitry responsivity. In an attempt to resolve controversy regarding the contributions of mesolimbic DA systems to reward, we review the three main competing explanatory categories: “liking”, “learning”, and “wanting”. They are (a) the hedonic impact -liking reward, (b) the ability to predict rewarding effects -learning and (c) the incentive salience of reward-related stimuli -wanting. In terms of acute effects, most of the evidence seems to favor the “surfeit theory”. Due to preferential dopamine release at mesolimbic-VTA-caudate-accumbens loci most drugs of abuse and Reward Deficiency Syndrome (RDS) behaviors have been linked to heightened feelings of well-being and hyperdopaminergic states.The “dopamine hypotheses” originally thought to be simple, is now believed to be quite complex and involves encoding the set point of hedonic tone, encoding attention, reward expectancy, and incentive motivation. Importantly, Willuhn et al. shows that in a self-administration paradigm, (chronic) excessive use of cocaine is caused by decreased phasic dopamine signaling in the striatum. In terms of chronic addictions, others have shown a blunted responsivity at brain reward sites with food, nicotine, and even gambling behavior. Finally, we are cognizant of the differences in dopaminergic function as addiction progresses and argue that relapse may be tied to dopamine deficiency. Vulnerability to addiction and relapse may be the result of the cumulative effects of dopaminergic and other neurotransmitter genetic variants and elevated stress levels. We therefore propose that dopamine homeostasis may be a preferred goal to combat relapse.

Published on: October 23, 2015
doi: 10.17756/jrds.2015-016
Citation: Blum K, Thanos PK, Oscar-Berman M, Febo M, Baron D, et al. 2015. Dopamine in the Brain: Hypothesizing Surfeit or Deficit Links to Reward and Addiction. J Reward Defic Syndr 1(3): 95-104.