Reward mechanisms in the brain and their role in dependence: evidence from neurophysiological and neuroimaging studies

Martin‐Soelch, Chantal; Leenders, Klaus L.; Chevalley, AF; Missimer, John; Künig, G.; Magyar, S; Mino, Annie; Schultz, Willibrordus Weijmar

doi:10.1016/s0165-0173(01)00089-3

Cited by 134 publications

(104 citation statements)

References 36 publications

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“…Drugs k Dopaminergic transmission in the NAc and other mesolimbic reward pathways (Solomon and Corbit, 1974;Koob and Le Moal, 2001) k Motivation towards normally pleasurable stimuli (Grigson and Twining, 2002) k Activity in the NAc and other mesolimbic reward pathways Little et al, 1999;MartinSoelch et al, 2001a;Martin-Soelch et al, 2001b;Martin-Solch et al, 2001;Volkow et al, 2002a) Anhedonia and other negative affective states (Gawin and KhalsaDenison, 1996;Koob and Le Moal, 2001) commonly occurring in the setting of cortisol decreases during SGAs treatment Mann et al, 2006).…”

Section: Stress Exposure Also Affects Eating Habitsmentioning

confidence: 99%

“…Neuroimaging findings k Responsivity to natural rewards (summarized in Table 2) k In basal activity and in responsivity to drugs and natural rewards Little et al, 1999;Martin-Soelch et al, 2001a;Martin-Soelch et al, 2001b;Martin-Solch et al, 2001;Volkow et al, 2002a) Putative mechanisms k In tonic dopamine (Moore et al, 1999) owing to k in basal cortical dopaminergic and glutamatergic output (Lieberman et al, 1997;Laruelle, 2000;West et al, 2003) Altered tonic/phasic dopamine interaction caused by repeated drug administration (Grace, 2000;Goto and Grace, 2005) Motivational correlates k Sensitivity and responsivity to natural rewards and reinforcers (Table 2), that is, 'reward deficiency' (Comings and Blum, 2000) k Sensitivity and responsivity to natural rewards and reinforcers (Volkow et al, 2004a, b), that is, 'reward deficiency' (Comings and Blum, 2000) mActivity…”

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

138

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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Section: Stress Exposure Also Affects Eating Habitsmentioning

confidence: 99%

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

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“…For nicotine and other psychostimulant drugs of abuse, the accumulation of evidence supports the hypothesis that mesocorticolimbic dopamine (DA) systems mediate the reinforcement for continued drug use despite the harmful consequences. [3][4][5][6]10,11 Useful hypothesis of dopamine signaling in reward-based behaviors Rewards obtained from the environment serve as positive reinforcers that shape behaviors for success. Rewards provide the incentive to achieve goals that can yield pleasure and perpetuate life.…”

mentioning

confidence: 99%

“…11,14 The firing of DA neurons changes based on the difference between the actual and the expected reward. The DA neurons indicate the deviation of the environmental input from the animal's expectations, which developed based upon previous experience in the environment (learning).…”

mentioning

confidence: 99%

“…A wide range of studies, including electrical self-stimulation, selfadministration, place preference, in vivo imaging, pharmacology, and cellular electrophysiology have indicated that the neurotransmitter, DA, participates in these reward-based events. [3][4][5][6]10,11 Dopaminergic projections originating in the ventral tegmental area (VTA) and innervating the striatum, the amygdala, and the prefrontal cortex compose the mesocorticolimbic DA systems that have been specifically identified to be of primary, but not exclusive, importance.…”

mentioning

confidence: 99%

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Roles of dopamine signaling in nicotine addiction

Dani¹

2003

Mol Psychiatry

122

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More than 3 million deaths a year are attributable to smoking worldwide, and the use of tobacco is on the rise in developing countries. Consequently, tobacco use is one of the few causes of mortality that is increasing, with deaths projected to reach 10 million annually in 30-40 years. 1 In developed countries, smoking is presently estimated to cause 20% of all deaths, making it the largest single cause of preventable death. In the United States alone, smokingrelated illness causes more than 430 000 deaths and $150 billion in medical costs and lost productivity annually. 2 Nicotine is the primary addictive component of tobacco. [3][4][5][6][7] It motivates smoking by about 1.1 billion people, representing approximately one-third of the global population aged 15 and over. 8 The addictive power of tobacco is exemplified by the difficulty in quitting. Most attempts to quit smoking fail, and success is usually achieved only after repeated attempts. In the United States, nearly three-fourth of adult smokers want to stop. About one-third of these smokers try to quit each year, but only a few percent succeed. 9 Since it is such a serious health problem, nicotine addiction arising from tobacco use has been the focus of much research. For nicotine and other psychostimulant drugs of abuse, the accumulation of evidence supports the hypothesis that mesocorticolimbic dopamine (DA) systems mediate the reinforcement for continued drug use despite the harmful consequences. [3][4][5][6]10,11 Useful hypothesis of dopamine signaling in reward-based behaviors Rewards obtained from the environment serve as positive reinforcers that shape behaviors for success. Rewards provide the incentive to achieve goals that can yield pleasure and perpetuate life. Since the environment is variable and achieving desirable goals requires continual adjustments, rewards serve in an ongoing learning process that updates an animal's repertoire of behaviors. Exploiting the environment to achieve the natural rewards of food, shelter and, ultimately, reproductive success has evolutionarily produced important systems in the brain for the processing of reward-based learning. A wide range of studies, including electrical self-stimulation, selfadministration, place preference, in vivo imaging, pharmacology, and cellular electrophysiology have indicated that the neurotransmitter, DA, participates in these reward-based events. 3-6,10,11 Dopaminergic projections originating in the ventral tegmental area (VTA) and innervating the striatum, the amygdala, and the prefrontal cortex compose the mesocorticolimbic DA systems that have been specifically identified to be of primary, but not exclusive, importance.Addictive drugs tap into the reward-related neuronal systems, reinforcing and ultimately solidifying maladaptive behaviors. Years of experimentation have indicated that drugs such as cocaine, amphetamine, and nicotine mediate their reinforcing properties via the mesocorticolimbic DA systems. These drugs are self-administered in controlled animal studies, and the ...

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Neural Signatures of Cognitive Flexibility and Reward Sensitivity Following Nicotinic Receptor Stimulation in Dependent Smokers

et al. 2017

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Reward mechanisms in the brain and their role in dependence: evidence from neurophysiological and neuroimaging studies

Cited by 134 publications

References 36 publications

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

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

Roles of dopamine signaling in nicotine addiction

Neural Signatures of Cognitive Flexibility and Reward Sensitivity Following Nicotinic Receptor Stimulation in Dependent Smokers

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