Document Detail

Serotonin neurotransmission in anorexia nervosa.
MedLine Citation:
PMID:  22854305     Owner:  NLM     Status:  In-Data-Review    
Patients with anorexia nervosa (AN) show extreme dieting weight loss, hyperactivity, depression/anxiety, self-control, and behavioral impulsivity. 5-Hydroxytryptamine (5-HT; serotonin) is involved in almost all the behavioral changes observed in AN patients. Both genetic and environmental factors contribute toward the pathogenesis of AN. It is a frequent disorder among adolescent girls and young women and starts as an attempt to lose weight to look beautiful and attractive. Failure to see the turning point when fasting becomes unreasonable leads to malnutrition and AN. Tryptophan, the precursor of serotonin and an essential amino acid, is only available in the diet. It is therefore likely that excessive diet restriction and malnutrition decrease brain serotonin stores because the precursor is less available to the rate-limiting enzyme of 5-HT biosynthesis, which normally exists unsaturated with its substrate. Evidence shows that diet restriction-induced exaggerated feedback control over 5-HT synthesis and the smaller availability of tryptophan decreases serotonin neurotransmission at postsynaptic sites, leading to hyperactivity, depression, and behavioral impulsivity. A compensatory upregulation of postsynaptic 5-HT-1A receptors and hypophagic serotonin receptors may be involved in anxiety and suppression of appetite. It is suggested that tryptophan supplementation may improve pharmacotherapy in AN.
Darakhshan Jabeen Haleem
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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:  478-95     Citation Subset:  IM    
Neuroscience Research Laboratory, Dr Panjwani Center for Molecular Medicine & Drug Research, University of Karachi, Karachi, Pakistan.
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