The role of dopamine in the pursuit of nutritional value

McCutcheon, James E.

doi:10.1016/j.physbeh.2015.05.003

Cited by 33 publications

(28 citation statements)

References 96 publications

(157 reference statements)

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“…The activity of the hunger hormone ghrelin and orexin modulates food- and food-cue NAc dopamine responses (Cone et al . 2014, Cone et al 2015, McCutcheon 2015), providing a potential mechanism for the need-based modulation of cue-evoked dopamine signaling detected here. It is interesting that the cue-evoked dopamine signaling was modified by satiety without the requirement to re-experience (i.e., re-taste) the predicted foods in the novel sated state.…”

Section: Discussionmentioning

confidence: 77%

Nucleus accumbens core dopamine signaling tracks the need‐based motivational value of food‐paired cues

Aitken¹,

Greenfield²,

Wassum³

2016

Journal of Neurochemistry

104

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Environmental reward-predictive stimuli provide a major source of motivation for instrumental reward-seeking activity and this has been linked to dopamine signaling in the nucleus accumbens (NAc). This cue-induced incentive motivation can be quite general, not restricted to instrumental actions that earn the same unique reward, and is also typically regulated by one’s current need state, such that cues only motivate actions when this is adaptive. But it is unknown whether cue-evoked dopamine signaling is similarly regulated by need state. Here we used fast-scan cyclic voltammetry to monitor dopamine concentration changes in the NAc core of rats during a Pavlovian-to-instrumental transfer (PIT) task in which the motivating influence of two cues, each signaling a distinct food reward (sucrose or food pellets), over an action earning a third unique food reward (grape-flavored polycose) was assessed in a state of hunger and of satiety. Both cues elicited a robust NAc dopamine response when hungry. The magnitude of the sucrose cue-evoked dopamine response correlated with the PIT effect that was selectively induced by this stimulus. Satiety attenuated these cue-evoked dopamine responses and behavioral responding, even though rats had never experienced the specific food rewards in this state. These data demonstrate that cue-evoked NAc core responses are sensitive to current need state, one critical variable that determines the current adaptive utility of cue-motivated behavior.

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Section: Discussionmentioning

confidence: 77%

Nucleus accumbens core dopamine signaling tracks the need‐based motivational value of food‐paired cues

Aitken¹,

Greenfield²,

Wassum³

2016

Journal of Neurochemistry

104

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“…Several studies using microdialysis or fast‐scan voltammetry report an increase in dopamine release in the NAc during consumption or intra‐oral injection of sweet solutions (Hajnal & Norgren, ; Bassareo et al ., ; Hajnal et al ., ; Roitman et al ., ). Interestingly, changes in dopamine levels are higher for sucrose than for non‐caloric sweet rewards in food‐deprived animals (de Araujo et al ., ; Beeler et al ., ; McCutcheon, ) and can be transferred to predictive cues (Day et al ., ), suggesting an involvement of the NAc dopamine signalling in associative and motivational processes. Conversely, the dopamine system does not seem to be involved in the hedonic treatment of food rewards.…”

Section: Discussionmentioning

confidence: 99%

Long‐lasting deficits in hedonic and nucleus accumbens reactivity to sweet rewards by sugar overconsumption during adolescence

Naneix

Darlot

Coutureau

et al. 2016

Eur J of Neuroscience

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Adolescence is a critical period characterized by major neurobiological changes. Chronic stimulation of the reward system might constitute an important factor in vulnerability to pathological development. In spite of the dramatic increase in the consumption of sweet palatable foods during adolescence in our modern societies, the long-term consequences of such exposure on brain reward processing remain poorly understood. Here, we investigated in rats the long-lasting effects of sugar overconsumption during their adolescence on their adult reactivity to the hedonic properties of sweet rewards. Adolescent rats with continuous access to 5% sucrose solution (from postnatal day 30-46) showed escalating intake. At adulthood (post-natal day 70), using two-bottle free choice tests, sucrose-exposed rats showed lower intake than non-exposed rats suggesting decreased sensitivity to the rewarding properties of sucrose. In Experiment 1, we tested their hedonic-related orofacial reactions to intraoral infusion of tasty solutions. We showed that sucrose-exposed rats presented less hedonic reactions in response to sweet tastes leaving the reactivity to water or quinine unaltered. Hence, in Experiment 2, we observed that this hedonic deficit is associated with lower c-Fos expression levels in the nucleus accumbens, a brain region known to play a central role in hedonic processing. These findings demonstrate that a history of high sucrose intake during the critical period of adolescence induces long-lasting deficits in hedonic treatment that may contribute to reward-related disorders.

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“…Interestingly, McCutcheon (2015) suggested that post-ingestive mechanisms occurring from nutrients in the gut could impact food consumption and behavioral conditioning. The physiological processes essential to these mechanisms are multifaceted and are thought to join in mesolimbic DA signaling to translate post-ingestive sensing of nutrients that have a reinforcement reward value.…”

Section: Discussionmentioning

confidence: 99%

Pilot clinical observations between food and drug seeking derived from fifty cases attending an eating disorder clinic

Beitscher-Campbell¹,

Blum²,

Febo³

et al. 2016

J Behav Addict

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BackgroundThe reward deficiency syndrome hypothesis posits that genes are responsible for reward dependence and related behaviors. There is evidence that both bulimia and anorexia nervosa, especially in women, have been linked to a lifetime history of substance use disorder (SUD). There are difficulties in accepting food as an addiction similar to drugs; however, increasingly neuroimaging studies favor such an assertion.Case presentationsWe are reporting the evidence of comorbidity of eating disorders with SUD found within these case presentations. We show 50 case reports derived from two independent treatment centers in Florida that suggest the commonality between food and drug addictions. In an attempt to provide data from this cohort, many participants did not adequately respond to our questionnaire.DiscussionWe propose that dopamine agonist therapy may be of common benefit. Failure in the past may reside in too powerful D2 agonist activity leading to D2 receptor downregulation, while the new methodology may cause a reduction of “dopamine resistance” by inducing “dopamine homeostasis.” While this is not a definitive study, it does provide some additional clinical evidence that these two addictions are not mutually exclusive.ConclusionCertainly, it is our position that there is an overlap between food- and drug-seeking behavior. We propose that the studies focused on an effort to produce natural activation of dopaminergic reward circuitry as a type of common therapy may certainly be reasonable. Additional research is warranted.

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The role of dopamine in the pursuit of nutritional value

Cited by 33 publications

References 96 publications

Nucleus accumbens core dopamine signaling tracks the need‐based motivational value of food‐paired cues

Nucleus accumbens core dopamine signaling tracks the need‐based motivational value of food‐paired cues

Long‐lasting deficits in hedonic and nucleus accumbens reactivity to sweet rewards by sugar overconsumption during adolescence

Pilot clinical observations between food and drug seeking derived from fifty cases attending an eating disorder clinic

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