Evidence of increased dopamine receptor signaling in food-restricted rats

Tsimberg, Yelena; Berman, Yemiliya; Yamamoto, Norio

doi:10.1016/s0306-4522(03)00227-6

Cited by 142 publications

(140 citation statements)

References 72 publications

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“…This is consistent with previous reports showing that food deprivation increases operant behavior (Eagle et al, 1999) independent of the work requirement to obtain rewards (Aberman and Salamone, 1999). Thus, food deprivation appears to have a general facilitatory effect on operant responding, independent of genotype, reward and work requirements, perhaps mediated by upregulation of D1 and D2 dopamine receptor activity (Carr et al, 2003). However, the magnitude of the food deprivation-induced increase in operant responding was significantly greater in DAT KD than WT mice.…”

Section: Mice With Chronically Elevated Dopamine Exhibited Enhanced Tsupporting

confidence: 91%

Mice with Chronically Elevated Dopamine Exhibit Enhanced Motivation, but not Learning, for a Food Reward

Cagniard

Balsam

Brunner

et al. 2005

Neuropsychopharmacol

235

158

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Dopamine has been critically implicated in learning and motivation, although its precise role remains to be determined. In order to investigate the involvement of dopamine in learning and motivation for a food reward, we used dopamine transporter knockdown mice (DAT KD) that have chronically elevated levels of extracellular dopamine. The present study demonstrates that chronically elevated dopamine enhances tendency to work for a food reward without apparent effects on Pavlovian and operant learning for this reward. The increase in dopamine is associated with elevated levels of dynorphin and Fos B expression in the dorsal caudate-putamen and the core but not the shell subregion of the nucleus accumbens. These data suggest that motivation to work, but not learning, for a food reward appears to be under the critical influence of tonic dopaminergic activity in discrete brain areas relevant for a reward-directed behavior.

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Section: Mice With Chronically Elevated Dopamine Exhibited Enhanced Tsupporting

confidence: 91%

Mice with Chronically Elevated Dopamine Exhibit Enhanced Motivation, but not Learning, for a Food Reward

Cagniard

Balsam

Brunner

et al. 2005

Neuropsychopharmacol

235

158

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“…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. The commonality of the circuitries is further supported by crosssensitization between palatable food with drugs and alcohol (Carr et al, 2003;Avena and Hoebel, 2003a, b;Avena et al, 2004). Palatable foods do not only engage dopaminergic reward system but also change it (Bello et al, 2002;Fetissov et al, 2002;Hajnal and Norgren, 2002;Bello et al, 2003).…”

Section: Neural and Motivational Changes In Schizophrenia And In Sudsmentioning

confidence: 99%

“…Satiety is associated with decreased reward function secondary to insulin and leptin actions in the NAc, LH, VTA, taste receptor cells, and cortical areas (Figlewicz, 2003a(Figlewicz, , b, 2004Fulton et al, 2004;Berthoud, 2004b) during caloric overflow signaled by these hormones, whereas caloric restriction, reflected in subjective sensation of hunger, increases food reward (Carr, 2002;Fulton et al, 2004) by augmenting dopaminergic (Carr et al, 2003) and opioidergic (Carr and Wolinsky, 1993) neurotransmissions.…”

Section: Central Mechanisms For Energy Balance and For Food Reward Acmentioning

confidence: 99%

“…Appetite, that is, incentive motivational drive to seek and consume food, is derived from interrelated psychobiological factors including food's rewarding properties, individual's homeostatic needs, and cognitive ability to favor alternative (to eating) behaviors (Saper et al, 2002;Hinton et al, 2004;Kelley, 2004b). Satiety is associated with decreased reward function secondary to insulin and leptin actions (Figlewicz, 2003a(Figlewicz, , b, 2004Berthoud, 2004b) during caloric overflow signaled by these hormones, whereas caloric restriction, reflected in subjective sensation of hunger, increases food reward (Carr, 2002;Fulton et al, 2004) by augmenting dopaminergic (Carr et al, 2003) and opioidergic (Carr and Wolinsky, 1993) neurotransmission. On the other hand, reward centers activation by high sugar and fat content palatable foods promotes desire 'to come back for more' by upregulating of hunger signaling (orexin, agouti-related protein), melanin concentrating hormone) in hypothalamic orexigenic networks and by blunting brain responses to the peripheral satiety hormones, insulin and leptin (Erlanson-Albertsson, 2005;Isganaitis and Lustig, 2005).…”

Section: Stress Exposure Also Affects Eating Habitsmentioning

confidence: 99%

“…Intermittent exposure m In activity in the NAc, that is, no habituation (Rada et al, 2004) mm In activity in the NAc, that is, sensitization (Steketee, 2003) K Food produces sensitization to drugs and alcohol (Avena and Hoebel, 2003a;Avena and Hoebel, 2003b) K Drugs produce sensitization to sugar (Avena and Hoebel, 2003a) K Drug sensitization is enhanced by food restriction (Carr et al, 2003) Opiates Acute exposure m In activity (Tanda and Di Chiara, 1998;Colantuoni et al, 2002) m In activity (Tanda and Di Chiara, 1998;Roth-Deri et al, 2003) Only limited human data (Ibanez-Rojo et al, 1993;Bencherif et al, 2005) are available on effects of food on opioid neurotransmission Repeated exposure Neuroadaptations in opioid receptors; signs and symptoms of opioid dependence (Colantuoni et al, 2002;Rada et al, 2004) Opioid dependence; neuroadaptations in opioid receptors (Zubieta et al, 1996;15945065;Bailey et al, 2005;Heinz et al, 2005) Glutamate Repeated exposure K k Performance on a cognitive task recruiting PFC K 'Hypofrontality' (Volkow et al, 1992;) during withdrawal at baseline and when exposed to natural reinforcers (Garavan et al, 2000) K m PFC activity when food-related stimuli are presented (Del Parigi et al, 2002) K m In activity during exposure to drugs or drugrelated cues (Wang et al, 1999;Garavan et al, 2000;Grant et al, 1996, Childress et al, 1999 Neuroimaging data on palatable food are presented for comparison purposes only; the nature of palatable foods' glutamatergic effects has not yet been elucidated…”

Section: Neuroimaging Findingsmentioning

confidence: 99%

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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

133

142

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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...

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Association of Brain Reward Learning Response With Harm Avoidance, Weight Gain, and Hypothalamic Effective Connectivity in Adolescent Anorexia Nervosa

et al. 2018

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Key PointsQuestionHow does brain response in participants with adolescent anorexia nervosa (AN) compare with healthy controls during taste reward conditioning?FindingsIn this cross-sectional multimodal brain imaging study of 56 female adolescents and young adults with AN and 52 matched controls, the AN group showed hyperactivation in the caudate head, nucleus accumbens, and insula compared with controls during a classical conditioning paradigm that has been associated with dopamine function. Orbitofrontal brain response in the AN group was positively associated with harm avoidance and striatal-hypothalamic connectivity but negatively associated with change in body mass index during treatment.MeaningsAltered brain reward response in adolescent AN may indicate altered dopamine function, may have a key role in AN’s specific pathophysiology, and should be explored as a target for biological treatments.

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Evidence of increased dopamine receptor signaling in food-restricted rats

Cited by 142 publications

References 72 publications

Mice with Chronically Elevated Dopamine Exhibit Enhanced Motivation, but not Learning, for a Food Reward

Mice with Chronically Elevated Dopamine Exhibit Enhanced Motivation, but not Learning, for a Food Reward

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

Association of Brain Reward Learning Response With Harm Avoidance, Weight Gain, and Hypothalamic Effective Connectivity in Adolescent Anorexia Nervosa

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