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Wednesday, February 29, 2012

The debate over dopamine's role in reward: the case for incentive salience and ANGELINA JOLIE!

(The article below by Dr. Kent Berridge on incentive motivation is one of the most important papers I have read on behavioral neuroscience. Nonetheless, when compared to other masters of motivational literature such as Tony Robbins and Zig Ziglar, one feels it needs an extra 'something' to keep your attention on the printed word and of course remind you of the magic of dopamine as you navigate through prose that is admittedly not as exciting as the 4th grade level writing style of  our two masters.) 

The debate over dopamine’s role in reward: the case for incentive salience AND ANGELINA JOLIE!

Kent C. Berridge 

Received: 21 March 2006 /Accepted: 20 August 2006 / Published online: 27 October 2006
# Springer-Verlag 2006/ unauthorized Angelina Jolie revision 29 Feb 2012


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.

Keywords Accumbens. Reward . Opioid . Dopamine, Basal forebrain . Aversion . Associative learning . Appetite Addiction, ANGELINA JOLIE!


Some questions endure for ages, faced by generation after generation. Neuroscientists hope the question, ‘What does dopamine do for reward?’ will not be among them, but it still prompts debate after several decades. Fortunately, the answers to the dopamine question are becoming better. A formal debate on dopamine’s role in reward was held at a Gordon conference on catecholamines in 2005. This article describes the incentive salience case presented in that debate, and compares it to other hypotheses. A debate stance can sometimes help clarify alternative views, and that is the hope here. Therefore, this article is not an exhaustive review of dopamine function. My goal is to provide a useful viewpoint and a critical evaluation oalternatives and to point to new evidence that seems crucial to any decision about what dopamine does for reward.

Dopamine’s causal role in reward

What does dopamine do in reward? This is in essence a question about causation. It asks what causal contribution is made by increases or decreases in dopamine neurotransmission to produce changes in reward-related psychology and behavior. In this article, our focus is on cause and consequence. How to assign causal status to brain events is a complicated issue, but it is not too much an oversimplification to suggest that in practice, the causal question of dopamine’s role in reward has been approached in several experimental ways. One approach is to ask ‘What specific reward function is lost?’ when dopamine neurotransmission is suppressed (e.g., by antagonist drugs, neurotoxin, or other lesions or genetic manipulations that reduce dopamine neurotransmission). That approach asks about dopamine’s role as a necessary cause for reward. It identifies what reward functions cannot be carried on without it. A different approach is to ask ‘What reward function is enhanced?’ by elevations in dopamine signaling (e.g., elevated by agonist drugs, brain stimulation, or hyperdopaminergic genetic mutation). That approach asks about dopamine’s role as a sufficient cause for reward. It asks what reward function a dopamine increase is able to enhance (when other conditions in the brain do not simultaneously change so much as to invalidate hopes of obtaining a specific answer). A third approach is to ask ‘What reward functions are coded?’ by the dopamine neural activations during reward events (e.g., by recording firing of dopamine or related limbic neurons, measuring extracellular dopamine release, or neuroimaging activation in target structures). This question asks about neural coding of function via correlation, often in the hope of inferring causation on the basis of observing correlated functions. Dopamine function is a multifaceted target, so it helps to combine these multiple approaches. What does it contribute to reward? Let’s put on the table the best answers that have survived until today and evaluate each hypothesis for dopamine’s role against the others. These include activation-sensorimotor hypotheses of effort, arousal and response vigor; the hedonia hypothesis of reward pleasure; reward learning hypotheses of associative stamping-in, teaching signals and prediction errors; and the incentive salience hypothesis of reward ‘wanting’. I will describe each of these hypotheses in turn. Then recent experiments that pit hedonia, reward learning, and incentive salience hypothesis against each other will be considered. Their results indicates that dopamine may more directly mediate reward ‘wanting’ than either ‘liking’ or learning about the same rewards.

 Activation-sensorimotor hypothesis

Activation-sensorimotor hypotheses posit dopamine to mediate general functions of action generation, effort, movement, and general arousal or behavioral activation (Dommett et al. 2005; Horvitz 2002; Robbins and Everitt 1982; Salamone et al. 1994; Stricker and Zigmond 1986). These ideas are captured by statements in the literature such as “Dopamine mediates the ‘working to obtain’ (i.e., tendency to work for motivational stimulus and overcome response constraints, activation for engaging in vigorous  instrumental actions).” (Salamone and Correa 2002, p. 17) or “this dopamine response could assist in preparing the animal to deal with the unexpected by promoting the switching of attentional and behavioral resources” (Redgrave et al. 1999, p. 151) and “functions of the central DA systems could be explained in terms of an ‘energetic’ construct (i.e., one that accounts for the vigor and frequency of behavioral output) of activation.” (Robbins and Everitt 2006, this issue). Those sensorimotor hypotheses have much to recommend them and are supported by substantial evidence. Neuroscientists agree that dopamine systems play roles in movement activation and control and attention and arousal (Albin et al. 1995; Dauer and Przedborski 2003; Redgrave et al. 1999; Salamone and Correa 2002; Salamone et al. 2005). As an example from the 2005 Gordon debate, Salamone and colleagues have convincingly shown that low-dose neuroleptics shift choices away from effortful toward easy tasks, even at the cost of a preferred reward. However, activation-sensorimotor hypotheses are very general in scope, which makes it difficult for them to explain specific aspects of reward. They do not attempt to give clear and specific explanations of why rewards are hedonically pleasant or learned about or sought after. By extension to dopamine’s role in drug addiction and related disorders, they do not attempt to explain why addicts become compulsively motivated to take drugs again. To explain reward-specific aspects of dopamine activation and of addictive drugs, we need hypotheses of dopamine function that address more reward-specific processes themselves. In short, activation, effort or sensorimotor function does not explain why dopamine effects are rewarding, predictive or motivating—even though general activation function may be valid and important. For the rest of this paper, therefore, I will accept that dopamine does have general sensorimotor-activation functions, and will not challenge those hypotheses. But the discussion must move beyond them for the purpose of understanding dopamine’s more specific contributions to reward. We must turn to specific reward hypotheses of what dopamine does.

Analysis of hedonia hypothesis

The hedonia hypothesis suggests that dopamine in nucleus accumbens essentially is a ‘pleasure neurotransmitter’. It was developed chiefly by Roy Wise and his colleagues in the 1970s and 1980s and became a very influential view. As Wise originally put it: “the dopamine junctions represent a synaptic way station...where sensory inputs are translated into the hedonic messages we experience as pleasure, euphoria or ‘yumminess’” (Wise 1980, p. 94). Continuing echoes of the hedonia hypothesis might perhaps still be heard in more recent neuroscience statements such as “Clearly, the mesocorticolimbic dopamine system is critical for psychostimulant activation and psychomotor stimulant reinforcement and plays a role in the reinforcing action of other drugs” (Koob and Le Moal 2006, p. 89) or “The ability of drugs of abuse to increase dopamine in nucleus accumbens underlies their reinforcing effects.” ............................

Well, you get the drift. For the real article, sadly without Angelina, go here.

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