  Substances of abuse are known to activate and disrupt neuronal circuits in
the brain reward system. We propose a simple and easily interpretable dynamical
systems model to describe the neurobiology of drug addiction that incorporates
the psychiatric concepts of reward prediction error (RPE), drug-induced
incentive salience (IST), and opponent process theory (OPT). Drug-induced
dopamine releases activate a biphasic reward response with pleasurable,
positive "a-processes" (euphoria, rush) followed by unpleasant, negative
"b-processes" (cravings, withdrawal). Neuroadaptive processes triggered by
successive intakes enhance the negative component of the reward response, which
the user compensates for by increasing drug dose and/or intake frequency. This
positive feedback between physiological changes and drug self-administration
leads to habituation, tolerance and eventually to full addiction. Our model
gives rise to qualitatively different pathways to addiction that can represent
a diverse set of user profiles (genetics, age) and drug potencies. We find that
users who have, or neuroadaptively develop, a strong b-process response to drug
consumption are most at risk for addiction. Finally, we include possible
mechanisms to mitigate withdrawal symptoms, such as through the use of
methadone or other auxiliary drugs used in detoxification.
