Differential responsiveness of dopamine transmission to food-stimuli in nucleus accumbens shell/core compartments

Bassareo, Valentina; Chiara, G. Di

doi:10.1016/s0306-4522(98)00583-1

Cited by 376 publications

(238 citation statements)

References 24 publications

Supporting

Mentioning

213

Contrasting

Unclassified

Order By: Relevance

“…The ability of VTA AmyR signaling to modulate DA signaling to these other sites remains untested, but represents an extremely important extension of the current results. For example, DA signaling in the NAc shell is relevant for many aspects of feeding and food reward (Baldo and Kelley, 2007;Bassareo and Di Chiara, 1999;Beyene et al, 2010). The dopaminergic projection from the VTA to the shell may also contribute to the intake-suppressive effects of VTA AmyR activation.…”

Section: Discussionmentioning

confidence: 99%

Amylin Modulates the Mesolimbic Dopamine System to Control Energy Balance

Mietlicki‐Baase

Reiner

Cone

et al. 2014

Neuropsychopharmacol

103

View full text Add to dashboard Cite

Amylin acts in the CNS to reduce feeding and body weight. Recently, the ventral tegmental area (VTA), a mesolimbic nucleus important for food intake and reward, was identified as a site-of-action mediating the anorectic effects of amylin. However, the long-term physiological relevance and mechanisms mediating the intake-suppressive effects of VTA amylin receptor (AmyR) activation are unknown. Data show that the core component of the AmyR, the calcitonin receptor (CTR), is expressed on VTA dopamine (DA) neurons and that activation of VTA AmyRs reduces phasic DA in the nucleus accumbens core (NAcC). Suppression in NAcC DA mediates VTA amylin-induced hypophagia, as combined NAcC D1/D2 receptor agonists block the intake-suppressive effects of VTA AmyR activation. Knockdown of VTA CTR via adeno-associated virus short hairpin RNA resulted in hyperphagia and exacerbated body weight gain in rats maintained on high-fat diet. Collectively, these findings show that VTA AmyR signaling controls energy balance by modulating mesolimbic DA signaling.

show abstract

Section: Discussionmentioning

confidence: 99%

Amylin Modulates the Mesolimbic Dopamine System to Control Energy Balance

Mietlicki‐Baase

Reiner

Cone

et al. 2014

Neuropsychopharmacol

103

View full text Add to dashboard Cite

show abstract

“…Consumption of palatable food (Hajnal et al, 2004) and drugs (Hernandez and Hoebel, 1988) activates dopamine transmission in the mesolimbic dopaminergic system, whereas repeated exposure to both stimuli decreases dopaminergic firing (Bassareo and Di Chiara, 1999;Nestler, 2004) in the same neural structures (ie, habituation and tolerance). Repeated intermittent exposure to food (Rada et al, 2005) or to drugs (Steketee, 2003) conversely results in sensitization, that is, increased dopaminergic release in the NAc.…”

Section: Neural and Motivational Changes In Schizophrenia And In Sudsmentioning

confidence: 99%

“…Their chronic consumption leads to neuroadaptations in opioid receptors accompanied by signs and symptoms of opioid dependence (Zubieta et al, 1996;Colantuoni et al, 2002;Bailey et al, 2005;Heinz et al, 2005). Only limited human data (Hajnal et al, 2004) via fast sensory and slow postingestive effects (Volkow and Wise, 2005) m In activity in the NAc (Hernandez and Hoebel, 1988;Breiter et al, 1997) via direct pharmacological effects Effects magnitude: foododrugs (Bassareo and Di Chiara, 1999;Volkow and Wise, 2005) Repeated exposure k In activity in the NAc, that is, habituation (Bassareo and Di Chiara, 1999); kD2 receptors, correlated with BMI (Wang et al, 2001) k In activity in the NAc (see Table 3), that is, tolerance (Nestler, 2004); kD2 receptors Volkow et al, 2001b) Time courses for habituation and tolerance may be different…”

Section: Neuroimaging Findingsmentioning

confidence: 99%

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Elman

Borsook

Lukas

2006

Neuropsychopharmacol

138

142

View full text Add to dashboard Cite

Obesity is highly prevalent among patients with schizophrenia and is associated with detrimental health consequences. Although excessive consumption of fast food and pharmacotherapy with such second-generation antipsychotic agents (SGAs) as clozapine and olanzapine has been implicated in the schizophrenia/obesity comorbidity, the pathophysiology of this link remains unclear. Here, we propose a mechanism based on brain reward function, a relevant etiologic factor in both schizophrenia and overeating. A comprehensive literature search on neurobiology of schizophrenia and of eating behavior was performed. The collected articles were critically reviewed and relevant data were extracted and summarized within four key areas: (1) energy homeostasis, (2) food reward and hedonics, (3) reward function in schizophrenia, and (4) metabolic effects of the SGAs. A mesolimbic hyperdopaminergic state may render motivational/incentive reward system insensitive to low salience/palatability food. This, together with poor cognitive control from hypofunctional prefrontal cortex and enhanced hedonic impact of food, owing to exaggerated opioidergic drive (clinically manifested as pain insensitivity), may underlie unhealthy eating habits in patients with schizophrenia. Treatment with SGAs purportedly improves dopamine-mediated reward aspects, but at the cost of increased appetite and worsened or at least not improved opiodergic capacity. These effects can further deteriorate eating patterns. Pathophysiological and therapeutic implications of these insights need further validation via prospective clinical trials and neuroimaging studies. INTRODUCTIONObesity has reached pandemic proportions and it is rapidly surpassing smoking as a number one killer in the industrialized world (Sturm, 2002;Skidmore and Yarnell, 2004). Its annual cost to the American society is staggering, and is estimated to be around $117 billion owing to related illnesses and loss of productivity (National Institute of Diabetes and Digestive and Kidney Diseases, 2005).In schizophrenia, obesity is twice as prevalent as in the general public, afflicting over half this patient population (Allison et al, 1999a;Dixon et al, 2000; American Diabetes Association, 2004;Marder et al, 2004;Wirshing, 2004). Besides negative psychosocial impacts (distorted selfesteem and societal stigmatization) and medications noncompliance, schizophrenics appear to be particularly susceptible to the detrimental medical sequelae of obesity such as the 'Metabolic Syndrome', which is a cluster of cardiovascular risk factors, including abdominal adiposity, insulin resistance, impaired, glucose tolerance, dyslipidemia, and hypertension (McKee et al, 1986;Mukherjee et al, 1996;Brown et al, 2000;Haupt and Newcomer, 2002;Ryan and Thakore, 2002;Ryan et al, 2003;Holt et al, 2004;Kohen, 2004;Marder et al, 2004;Lieberman et al, 2005).Excessive body weight gain (BWG) could be attributed to a constellation of endocrine, molecular, genetic, demographic, and lifestyle-related factors. Provided that a common tra...

show abstract

“…6 A baseline comparison of regional brain glucose metabolism between obese (Ob) and normal weight subjects revealed that even without FS, Ob subjects had significantly higher metabolism in the parietal somatosensory cortex where the lips and tongue are represented, which was interpreted to reflect increased sensitivity of the regions that process food palatability. 7 Studies in laboratory animals have also identified regional activation of the prefrontal cortex, 8 amygdala 9 and nucleus accumbens 10 upon exposure to rewarding food stimuli. Here, we evaluate the regional brain metabolic responses to a food stimulus to assess the brain response to food reinforcers.…”

Section: Introductionmentioning

confidence: 99%

Differences in response to food stimuli in a rat model of obesity: in-vivo assessment of brain glucose metabolism

et al. 2008

View full text Add to dashboard Cite

Objective: Food intake is regulated by factors that modulate caloric requirements as well as food's reinforcing properties. In this study, we measured brain glucose utilization to an olfactory stimulus (bacon scent), and we examined the role of food restriction and genetic predisposition to obesity on such brain metabolic activity. Methods: Zucker obese (Ob) and lean (Le) rats were divided into four groups: (1) Ob ad-libitum fed, (2) Ob food restricted (70% of ad libitum), (3) Le ad-libitum fed and (4) Le food restricted. Rats were scanned using m-positron emission tomography and 2-[ 18 F]-fluoro-2-deoxy-D-glucose under two conditions: (1) baseline scan (no stimulation) and (2) challenge scan (food stimulation, FS). Results: FS resulted in deactivation of the right and left hippocampus. Ob rats showed greater changes with FS than Le rats (deactivation of hippocampus and activation of the medial thalamus) and Ob but not Le animals deactivated the frontal cortex and activated the superior colliculus. Access to food resulted in an opposite pattern of metabolic changes to the food stimuli in olfactory nucleus (deactivated in unrestricted and activated in restricted) and in right insular/parietal cortex (activated in unrestricted and deactivated in restricted). In addition, restricted but not unrestricted animals activated the medial thalamus. Conclusions: The greater changes in the Ob rats suggest that leptin modulates the regional brain responses to a familiar food stimulus. Similarly, the differences in the pattern of responses with food restriction suggest that FS is influenced by access to food conditions. The main changes with FS occurred in the hippocampus, a region involved in memory, the insular cortex, a region involved with interoception (perception of internal sensations), the medial thalamus (region involved in alertness) and in regions involved with sensory perception (olfactory bulb, olfactory nucleus, occipital cortex, superior colliculus and parietal cortex), which corroborates their relevance in the perception of food.

show abstract

Differential responsiveness of dopamine transmission to food-stimuli in nucleus accumbens shell/core compartments

Cited by 376 publications

References 24 publications

Amylin Modulates the Mesolimbic Dopamine System to Control Energy Balance

Amylin Modulates the Mesolimbic Dopamine System to Control Energy Balance

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Differences in response to food stimuli in a rat model of obesity: in-vivo assessment of brain glucose metabolism

Contact Info

Product

Resources

About