Incentive salience: a motivational theory of addiciton
Cussen, Autumn M.
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Not all individuals who try a potentially addictive drug, or even a ‘hard drug’, become addicted. What causes the transition from ‘user’ to ‘addict’ in certain individuals has been long debated. The incentive salience hypothesis is one explanation to this question. According to this hypothesis, drugs cause many psychological changes in the brain. Of these changes, the most important is ‘sensitization’ or hypersensitivity to the incentive motivational effects of drugs and drug-associated stimuli. Incentive sensitization produces a bias of attentional processing towards drug-associated stimuli and a pathological motivation for drugs (compulsive ‘wanting’). Additionally, there are three psychological processes that compose incentive motivation and reward. Hedonic (pleasure) activation by a US (usually a reward, for addicts it’s the ‘drug high’), associative learning of the correlation between the cue CS and US, and attribution of incentive salience to the CS are all needed for incentive salience to occur. In this experiment, we used a non-specific dopamine antagonist, flupenthixol, to test the role of dopamine in reward and in incentive salience. If dopamine works in reward as the hypothesis predicts, then animals without dopamine would be able to produce hedonic responses and associative learning between the cue and reward but they would not be able to attribute incentive salience. Thus, once flupenthixol is removed animals should be able to perform all three aspects of the incentive salience hypothesis because none of the components are now blocked. Our results did not provide any significant results thus, future studies are needed to examine this hypothesis and its role in reward further.