The below 1998 dopamine pleasure versus wanting study abstract should be part of this thread as it is the earliest paper I've seen on the topic and provides the foundation science for much of the above. The word "hedonic" as used the below study summary means "of, relating to, or marked by pleasure."
Seventy percent of surveyed smokers state that they want to quit. Does that sound like smoking is about like, love or pleasure? But it's entirely normal when seeing ourselves do something over and over and over to think and feel that there must be some like, love or pleasure to it, or else why would we do it again? This line of research suggests that the urges felt are about satisfying dopamine pathway want and desire, not love, like or pleasure, that the "aaah" sensation sensed within ten seconds of a puff is actually relief from neuro-chemically generated want.
Although a lot to swallow, what's simple is knowing that it is impossible to relapse so long as no nicotine enters this bloodstream!
Breathe deep, hug hard, live long,
John (Gold x11)
What is the role of dopamine in reward:
hedonic impact, reward learning,
or incentive salience?
Journal: Brain Research. Brain Research Reviews, December 1998, Volume 28(3), Page 309-369.
Authors: Berridge KC, Robinson TE.
Department of Psychology, University of Michigan, Ann Arbor, MI 48109-1109, USA.email@example.com
"What roles do mesolimbic and neostriatal dopamine systems play in reward? Do they mediate the hedonic impact of rewarding stimuli? Do they mediate hedonic reward learning and associative prediction? Our review of the literature, together with results of a new study of residual reward capacity after dopamine depletion, indicates the answer to both questions is 'no'. Rather, dopamine systems may mediate the incentive salience of rewards, modulating their motivational value in a manner separable from hedonia and reward learning.
In a study of the consequences of dopamine loss, rats were depleted of dopamine in the nucleus accumbens and neostriatum by up to 99% using 6-hydroxydopamine. In a series of experiments, we applied the 'taste reactivity' measure of affective reactions (gapes, etc.) to assess the capacity of dopamine-depleted rats for: 1) normal affect (hedonic and aversive reactions), 2) modulation of hedonic affect by associative learning (taste aversion conditioning), and 3) hedonic enhancement of affect by non-dopaminergic pharmacological manipulation of palatability (benzodiazepine administration).
We found normal hedonic reaction patterns to sucrose vs. quinine, normal learning of new hedonic stimulus values (a change in palatability based on predictive relations), and normal pharmacological hedonic enhancement of palatability. We discuss these results in the context of hypotheses and data concerning the role of dopamine in reward. We review neurochemical, electrophysiological, and other behavioral evidence.
We conclude that dopamine systems are not needed either to mediate the hedonic pleasure of reinforcers or to mediate predictive associations involved in hedonic reward learning. We conclude instead that dopamine may be more important to incentive salience attributions to the neural representations of reward-related stimuli. Incentive salience, we suggest, is a distinct component of motivation and reward. In other words, dopamine systems are necessary for 'wanting' incentives, but not for 'liking' them or for learning new 'likes' and 'dislikes'."
PubMed Link: http://www.ncbi.nlm.nih.gov/pubmed/9858756
Below is a more recent paper by Berridge
The debate over dopamine's role in reward:
the case for incentive salience.
Psychopharmacology (Berlin). 2007 Apr;191(3):391-431. Epub 2006 Oct 27.
Department of Psychology, University of Michigan, 530 Church Street (East Hall), Ann Arbor, MI 48109, USA. [url=mailto:firstname.lastname@example.org
Abstract INTRODUCTION: Debate continues over the precise causal contribution made by mesolimbic dopamine systems to reward. There are three competing explanatory categories: 'liking', learning, and 'wanting'. Does dopamine mostly mediate the hedonic impact of reward ('liking')? Does it instead mediate learned predictions of future reward, prediction error teaching signals and stamp in associative links (learning)? Or does dopamine motivate the pursuit of rewards by attributing incentive salience to reward-related stimuli ('wanting')? Each hypothesis is evaluated here, and it is suggested that the incentive salience or 'wanting' hypothesis of dopamine function may be consistent with more evidence than either learning or 'liking'.
In brief, recent evidence indicates that dopamine is neither necessary nor sufficient to mediate changes in hedonic 'liking' for sensory pleasures. Other recent evidence indicates that dopamine is not needed for new learning, and not sufficient to directly mediate learning by causing teaching or prediction signals. By contrast, growing evidence indicates that dopamine does contribute causally to incentive salience. Dopamine appears necessary for normal 'wanting', and dopamine activation can be sufficient to enhance cue-triggered incentive salience. Drugs of abuse that promote dopamine signals short circuit and sensitize dynamic mesolimbic mechanisms that evolved to attribute incentive salience to rewards. Such drugs interact with incentive salience integrations of Pavlovian associative information with physiological state signals. That interaction sets the stage to cause compulsive 'wanting' in addiction, but also provides opportunities for experiments to disentangle 'wanting', 'liking', and learning hypotheses. Results from studies that exploited those opportunities are described here.
CONCLUSION: In short, dopamine's contribution appears to be chiefly to cause 'wanting' for hedonic rewards, more than 'liking' or learning for those rewards.
PMID: 17072591 [PubMed - indexed for MEDLINE]
PubMed Link: http://www.ncbi.nlm.nih.gov/pubmed/17072591