Role of brain dopamine in food reward and reinforcement

Intramural Research Program, Department of Health and Human Services, National Institute on Drug Abuse, Baltimore, MD 21224, USA.
Philosophical Transactions of The Royal Society B Biological Sciences (Impact Factor: 7.06). 08/2006; 361(1471):1149-58. DOI: 10.1098/rstb.2006.1854
Source: PubMed


The ability of food to establish and maintain response habits and conditioned preferences depends largely on the function of brain dopamine systems. While dopaminergic transmission in the nucleus accumbens appears sufficient for some forms of reward, the role of dopamine in food reward does not appear to be restricted to this region. Dopamine plays an important role in both the ability to energize feeding and to reinforce food-seeking behaviour; the role in energizing feeding is secondary to the prerequisite role in reinforcement. Dopaminergic activation is triggered by the auditory and visual as well as the tactile, olfactory, and gustatory stimuli of foods. While dopamine plays a central role in the feeding and food-seeking of normal animals, some food rewarded learning can be seen in genetically engineered dopamine-deficient mice.

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    • "Among these regions, the DA neuron system, which plays an important role in the regulation of reward and motivational behaviors, emerged as a potential target for insulin and leptin actions. The mesolimbic DA neurons project from the VTA and substantia nigra (SN) to the nucleus accumbens (NAc) and have been implicated in the rewarding and motivating aspects of food intake (Berridge, 1996; Saper et al., 2002; Kelley et al., 2005b; Wise, 2006). One of the factors contributing to increased incidences of obesity is diet composition especially in this modern era where most people opt for processed or instant foods. "
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    ABSTRACT: The central actions of leptin and insulin are essential for the regulation of energy and glucose homeostasis. In addition to the crucial effects on the hypothalamus, emerging evidence suggests that the leptin and insulin signaling can act on other brain regions to mediate the reward value of nutrients. Recent studies have indicated the midbrain dopaminergic neurons as a potential site for leptin' and insulin's actions on mediating the feeding behaviors and therefore affecting the energy balance. Although molecular details about the integrative roles of leptin and insulin in this subset of neurons remain to be investigated, substantial body of evidence by far imply that the signaling pathways regulated by leptin and insulin may play an essential role in the regulation of energy balance through the control of food-associated reward. This review therefore describes the convergence of energy regulation and reward system, particularly focusing on leptin and insulin signaling in the midbrain dopaminergic neurons.
    Frontiers in Psychology 08/2014; 5:846. DOI:10.3389/fpsyg.2014.00846 · 2.80 Impact Factor
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    • "In the mammalian brain, midbrain dopaminergic cells project widely to both cortical and subcortical regions, forming the mesocortical, mesolimbic and nigrostriatal DA systems. These widespread dopaminergic projections provide the primary source of DA to the brain and the dynamic shift from tonic to phasic DA cell firing and transmitter release is thought to modulate brain function to signal stimulus salience of both artificial and natural reinforcers, and to enhance learning of behavioral responses toward such reinforcers (Wise 2006; Schultz 2010). To signal salience , DA neurons switch from an irregular single-spike firing to phasic burst-like firing, which results in increased extracellular DA in the target regions (Schultz 1998; Phillips et al. 2003). "
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    ABSTRACT: Although the importance of the medial prefrontal cortex (MPFC) in cocaine addiction is well established, its precise contribution to cocaine seeking, taking and relapse remains incompletely understood. In particular, across two different models of cocaine self-administration, pharmacological or optogenetic activation of the dorsal MPFC has been reported to sometimes promote and sometimes inhibit cocaine seeking. We highlight important methodological differences between the two experimental paradigms and propose a framework to potentially reconcile the apparent discrepancy. We also draw parallels between these pre-clinical models of cocaine self-administration and human neuro-imaging studies in cocaine users, and argue that both lines of evidence point to dynamic interactions between cue-reactivity processes and control processes within the dorsal MPFC circuitry. From a translational perspective, these findings underscore the importance of interventions and therapeutics targeting not just a brain region, but a specific computational process within that brain region, and may have implications for the design and implementation of more effective treatments for human cocaine addiction.
    Addiction Biology 03/2014; 20(2). DOI:10.1111/adb.12132 · 5.36 Impact Factor
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    • "It is currently unclear whether the mesolimbic system plays a role in the hedonic-driven food consumption [7], [10], [11]. The mesolimbic system is activated in response to palatable foods, and dopamine release in the NAc augments the drive to obtain food rewards [12]–[14]. However, NAc dopamine depletion alone does not alter feeding, and pharmacological blockade of dopamine receptors in the NAc affects motor behavior and has no effects on food intake [13], [15]. "
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    ABSTRACT: Overconsumption of palatable energy-dense foods has negative health implications and it is associated with obesity and several eating disorders. Currently, little is known about the neuronal circuitries activated by the acute ingestion of a rewarding stimulus. Here, we used a combination of immunohistochemistry, pharmacology and neuronal tracing analyses to examine the role of the mesolimbic system in general, and the orexin neurons in particular, in a simple experimental test in which naïve mice are allowed to spontaneously eat a pellet of a high fat diet (HFD) for 2 h. We found that acute HFD activates c-Fos expression in several reward-related brain areas, including the ventral tegmental area (VTA), nucleus accumbens, central amygdala and lateral hypothalamic area. We also found that: i- HFD-mediated orosensory stimulation was required for the mesolimbic pathway activation, ii- acute HFD differentially activates dopamine neurons of the paranigral, parabrachial pigmented and interfascicular sub-regions of the VTA, and iii- orexin neurons of the lateral hypothalamic area are responsive to acute HFD. Moreover, orexin signaling blockade, with the orexin 1 receptor antagonist SB-334867, reduces acute HFD consumption and c-Fos induction in the VTA but not in the other mesolimbic nuclei under study. Finally, we found that most orexin neurons responsive to acute HFD innervate the VTA. Our results show that acute HFD consumption recruits the mesolimbic system and that the full manifestation of this eating behavior requires the activation of orexin signaling.
    PLoS ONE 01/2014; 9(1):e87478. DOI:10.1371/journal.pone.0087478 · 3.23 Impact Factor
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