Those affective facial expressions to taste are homologous in human infants, apes and monkeys, and even rats ( Grill & Norgren, 1978 Steiner, Glaser, Hawilo, & Berridge, 2001). Sweetness elicits relaxed facial expressions and rhythmic tongue and mouth expressions of ‘liking’, whereas bitterness elicits ‘disgust’ gapes and turning away. We used a naturalistic or ethological assay of sweetness pleasure, based on affective facial expressions of ‘liking’ ( Steiner, 1973). Our approach to measuring pleasure impact was different, and more similar to how for millennia parents have asked their newborn infants whether the taste of a particular food was enjoyable.
Changes in ‘wanting’ were naturally interpreted to reflect corresponding changes in ‘liking’, based on the assumption that ‘wanting’ was proportional to ‘liking’. Our early experiment was simply intended to provide another bit of evidence for the dopamine-pleasure hypothesis - but results turned out otherwise.Īs background, many studies had found that brain dopamine systems were activated by most rewards, and further that manipulating dopamine altered ‘wanting’ for rewards: for example changing how much animals preferred, pursued, worked for, or consumed the reward ( Koob & Le Moal, 1997 Wise, 1985). At the time, we and most other investigators generally accepted the idea that dopamine mediates reward pleasure: the hedonic impact of tasty food, addictive drugs and many other rewards.
However, that idea, which we first proposed in 1989 as a post hoc explanation for some negative results on the role of the brain’s mesolimbic dopamine system in pleasure ( Berridge et al 1989), originally came as a surprise even to us. It is now widely accepted that brain mechanisms that determine how much a reward is ‘wanted’ are dissociable from those that determine how much the same reward is ‘liked’. Further, its scope is now expanding to include diverse behavioral addictions and other psychopathologies. A quarter-century after its proposal, evidence has continued to grow in support the incentive-sensitization theory. This is due to long-lasting changes in dopamine-related motivation systems of susceptible individuals, called neural sensitization. The incentive-sensitization theory posits the essence of drug addiction to be excessive amplification specifically of psychological ‘wanting’, especially triggered by cues, without necessarily an amplification of ‘liking’. By comparison, ‘liking’, or the actual pleasurable impact of reward consumption, is mediated by smaller and fragile neural systems, and is not dependent on dopamine. Incentive salience or ‘wanting’, a form of motivation, is generated by large and robust neural systems that include mesolimbic dopamine. However, the brain circuitry that mediates the psychological process of ‘wanting’ a particular reward is dissociable from circuitry that mediates the degree to which it is ‘liked’. Rewards are both ‘liked’ and ‘wanted’, and those two words seem almost interchangeable.
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