Endorphins, Dopamine, and Schizophrenia*

Volavka, Jan; Davis, Leonard G.; Ehrlich, Yigal H.

doi:10.1093/schbul/5.2.227

Cited by 80 publications

(22 citation statements)

References 80 publications

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“…Endogenous opioid system disturbances have been observed in schizophrenia. The excess of endorphins in schizophrenia is one of the postulated hypothesis . In our previous study, we also found about 20% higher BE concentration in patients with schizophrenia than in healthy controls .…”

Section: Introductionmentioning

confidence: 56%

Overrated hedonic judgment of odors in patients with schizophrenia

2018

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There is potential relationship between increased β-endorphin concentration and severity of negative symptoms. Patients with predominant negative symptoms tend to evaluate odors as significantly more pleasant. Individuals with this subtype of schizophrenia might present specific, altered pattern of smell identification and hedonic judgment. Presumably, β-endorphin has no direct influence on olfactory identification performance and hedonic judgment in schizophrenia.

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Section: Introductionmentioning

confidence: 56%

Overrated hedonic judgment of odors in patients with schizophrenia

2018

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“…Opioid peptides modulate dopaminergic synaptic transmission by exerting both presynaptic and postsynaptic effects; this modulation may involve the activity of nucleotide cyclases and protein phosphorylation systems [9]. Thus, dopaminergic neuronal hyperactivity, currently believed to be related to schizophrenia, might be caused by a primary alteration in the endorphin system.…”

Section: Resultsmentioning

confidence: 99%

“…However, no mutations in dopamine receptors have been clearly associated with disease [5,6]. This lack of evidence has directed efforts towards the examination of defects in dopamine metabolism and/or signal transduction within dopamine pathways including the interaction of dopamine with other neurotransmitter systems as neurotrophic factors [7], cytokines [8], and opioid peptides [9].…”

Section: Introductionmentioning

confidence: 99%

Allelic Variation in the Human Prodynorphin Gene Promoter and Schizophrenia

et al. 2002

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Experimental and clinical studies suggest an involvement of the opioid neuropeptide system in schizophrenia. In particular, the prodynorphin (PDYN), the precursor of the dynorphin opioid peptides, has been shown to play an important role in several aspects of human mental diseases. Recently, a functional polymorphism in the promoter of PDYN gene has been described. We studied the possible relationship between this polymorphism and schizophrenia and we found no significant difference in allelic and genotype distributions between schizophrenic patients and control subjects. However, we observed a significant interactive effect with the receptor 3 of dopamine gene (DRD3); in particular, the frequency of subjects carrying PDYN allele 3 being also homozygotes for DRD3 Gly allele (of Ser9Gly polymorphism) was significantly greater in patients than controls. We conclude that PDYN gene polymorphism alone does not alter the risk for schizophrenia but, by an epistatic interaction with the Gly allele of DRD3 gene, may contribute to the susceptibility to this disorder.

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“…Opiates levels tend to parallel the severity of psychosis (Terenius et al, 1976;Lindstrom et al, 1978;Rimon et al, 1980;Marchesi et al, 1995), suggesting involvement of this neurochemical effect in schizophrenia neuropathology (Volavka et al, 1979;Schmauss and Emrich, 1985;Nemeroff and Bissette, 1988).…”

Section: Abnormal Opioidergic Function May Impair Liking Processes Inmentioning

confidence: 99%

“…On the basis of the hypothesis that opioidergic mechanisms are involved in the pathophysiology and symptoms of schizophrenia (Volavka et al, 1979;Schmauss and Emrich, 1985;Nemeroff and Bissette, 1988), opioid antagonists were evaluated for potential antipsychotic efficacy in numerous clinical trials (McNicholas and Martin, 1984;Nemeroff and Bissette, 1988;Welch and Thompson, 1994). On the whole, they were safe and well tolerated and resulted in significant improvements of various aspects of schizophrenic symtomatology such as positive and deficit symptoms, polydipsia, alcoholism, and tardive dyskinesia in some (Watson et al, 1978;Lehmann et al, 1979;Berger et al, 1981;Nishikawa et al, 1994a, b;Marchesi et al, 1995;Petrakis et al, 2004;Wonodi et al, 2004), but not all (Volavka et al, 1977;Pickar et al, 1982) participants.…”

Section: Opioid Antagonists May Improve Hedonic Deficits In Patients mentioning

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

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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Endorphins, Dopamine, and Schizophrenia*

Cited by 80 publications

References 80 publications

Overrated hedonic judgment of odors in patients with schizophrenia

Overrated hedonic judgment of odors in patients with schizophrenia

Allelic Variation in the Human Prodynorphin Gene Promoter and Schizophrenia

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

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