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