Document Detail


Assessment of 5-hydroxytryptamine efflux in rat brain during a mild, moderate and severe serotonin-toxicity syndrome.
MedLine Citation:
PMID:  19464285     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Serotonin (5-hydroxytryptamine; 5-HT)-toxicity syndrome, an iatrogenic brain disorder induced by excessive efflux of 5-HT, has received much attention because of increasing incidents of serotonergic antidepressants. However, the neural mechanism by which extracellular 5-HT is elevated to a toxic level for the syndrome remains to be determined. The goal of the present study was to test the hypothesis that extracellular 5-HT is composed of two component effluxes responsible for distinct aspects of the syndrome. The first set of experiments was to characterize the syndrome by measuring changes in neuromuscular signs, body-core temperature and mortality rate. Our results indicate that the syndrome severity can be categorized into mild, moderate and severe levels. The second set of experiments was to determine a threshold of extracellular 5-HT for induction of each level of the syndrome. Our results demonstrate that there were an 11-fold increase in the mild syndrome and an over 55-fold increase in the severe syndrome. In the last series of experiments, the excessive increases in 5-HT were pharmacologically separated into primary and secondary component effluxes with the 5-HT2A receptor antagonists cyproheptadine and ketanserin and NMDA receptor antagonist (+)-MK-801. Our results suggest that the primary component efflux was caused by direct drug effects on 5-HT biosynthetic and metabolic pathways and secondary efflux ascribed to indirect drug effect on a positive-feedback circuit involving 5-HT2A and NMDA receptors. In summary, the primary efflux could be an initial cause for the induction of the syndrome while the secondary efflux might involve deterioration of the syndrome.
Authors:
Gongliang Zhang; Swapna Krishnamoorthy; Zhiyuan Ma; Nick P Vukovich; Xupei Huang; Rui Tao
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-05-20
Journal Detail:
Title:  European journal of pharmacology     Volume:  615     ISSN:  1879-0712     ISO Abbreviation:  Eur. J. Pharmacol.     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-06-26     Completed Date:  2009-11-10     Revised Date:  2010-09-27    
Medline Journal Info:
Nlm Unique ID:  1254354     Medline TA:  Eur J Pharmacol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  66-75     Citation Subset:  IM    
Affiliation:
Charles E. Schmidt College of Biomedical Science, Florida Atlantic University, 777 Glades Road, Boca Raton, Florida 33431, USA.
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MeSH Terms
Descriptor/Qualifier:
5-Hydroxytryptophan / metabolism*
Animals
Antidepressive Agents / toxicity
Body Temperature / drug effects
Clorgyline / toxicity
Cyproheptadine / pharmacology
Disease Models, Animal
Dizocilpine Maleate / pharmacology
Dose-Response Relationship, Drug
Ketanserin / pharmacology
Male
Microdialysis
Prefrontal Cortex / drug effects*,  metabolism
Rats
Rats, Sprague-Dawley
Receptor, Serotonin, 5-HT2A / antagonists & inhibitors
Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors
Serotonin / metabolism*
Serotonin Syndrome / chemically induced,  metabolism*,  physiopathology
Grant Support
ID/Acronym/Agency:
DA14541/DA/NIDA NIH HHS; R01 DA014541-06/DA/NIDA NIH HHS
Chemical
Reg. No./Substance:
0/Antidepressive Agents; 0/Receptor, Serotonin, 5-HT2A; 0/Receptors, N-Methyl-D-Aspartate; 129-03-3/Cyproheptadine; 17780-72-2/Clorgyline; 50-67-9/Serotonin; 56-69-9/5-Hydroxytryptophan; 74050-98-9/Ketanserin; 77086-22-7/Dizocilpine Maleate
Comments/Corrections

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