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Dopamine in anorexia nervosa: a systematic review.
MedLine Citation:
PMID:  22854306     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Anorexia nervosa (AN) is a chronic relapsing psychiatric disorder with a largely unknown pathophysiology. Dopamine has been implicated in the pathophysiology of the disorder by preclinical and clinical evidence. Preclinical studies have examined two main characteristics of AN: reduction in food intake (diet restriction) and hyperactivity. Diet restriction has been associated with reduced dopamine levels in the hypothalamus, hippocampus, and the dorsal striatum. Animal hyperactivity following diet restriction has been linked to increased dopamine in the hypothalamus. Increased dopamine in the nucleus accumbens was associated with food administration, but not food expectation. Tyrosine and dopaminergic antagonists normalized anorexia-like behaviors in animal models of AN, but did not restore body weight. Clinical studies on the etiology of AN have produced contradictory findings. Cerebrospinal fluid concentrations of dopamine and its metabolites have been reported to be decreased or normal under conditions of low weight, whereas they tended to normalize when the weight was restored. Plasma and urinary levels of dopamine and its metabolites have been found to be normal, increased, and decreased. Neuroendocrine studies suggest that dopaminergic neurotransmission is increased in AN. However, recent neuroimaging studies lend support to the increase in binding of dopaminergic receptors in the striatum, which favors the opposite theory that intrasynaptic dopamine is indeed decreased. Genetic studies implicate dopamine D2 receptors, the dopamine transporter, and the enzyme COMT. There are promising results with respect to the use of atypical antipsychotics against symptoms of AN beyond weight gain, but further trials are required.
Authors:
Dimitrios Kontis; Eirini Theochari
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Behavioural pharmacology     Volume:  23     ISSN:  1473-5849     ISO Abbreviation:  Behav Pharmacol     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-08-02     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9013016     Medline TA:  Behav Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  496-515     Citation Subset:  IM    
Affiliation:
Unit for the Study of Cognition in Psychosis, Psychiatric Hospital of Attica, Athens, Greece.
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