Document Detail


The neurobiology of retinoic acid in affective disorders.
MedLine Citation:
PMID:  17707566     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Current models of affective disorders implicate alterations in norepinephrine, serotonin, dopamine, and CRF/cortisol; however treatments targeted at these neurotransmitters or hormones have led to imperfect resolution of symptoms, suggesting that the neurobiology of affective disorders is incompletely understood. Until now retinoids have not been considered as possible contributors to affective disorders. Retinoids represent a family of compounds derived from vitamin A that perform a large number of functions, many via the vitamin A product, retinoic acid. This signaling molecule binds to specific retinoic acid receptors in the brain which, like the glucocorticoid and thyroid hormone receptors, are part of the nuclear receptor superfamily and regulate gene transcription. Research in the field of retinoic acid in the CNS has focused on the developing brain, in part stimulated by the observation that isotretinoin (13-cis retinoic acid), an isomer of retinoic acid used in the treatment of acne, is highly teratogenic for the CNS. More recent work has suggested that retinoic acid may influence the adult brain; animal studies indicated that the administration of isotretinoin is associated with alterations in behavior as well as inhibition of neurogenesis in the hippocampus. Clinical evidence for an association between retinoids and depression includes case reports in the literature, studies of health care databases, and other sources. A preliminary PET study in human subjects showed that isotretinoin was associated with a decrease in orbitofrontal metabolism. Several studies have shown that the molecular components required for retinoic acid signaling are expressed in the adult brain; the overlap of brain areas implicated in retinoic acid function and stress and depression suggest that retinoids could play a role in affective disorders. This report reviews the evidence in this area and describes several systems that may be targets of retinoic acid and which contribute to the pathophysiology of depression.
Authors:
J Douglas Bremner; Peter McCaffery
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Publication Detail:
Type:  Journal Article; Review     Date:  2007-07-10
Journal Detail:
Title:  Progress in neuro-psychopharmacology & biological psychiatry     Volume:  32     ISSN:  0278-5846     ISO Abbreviation:  Prog. Neuropsychopharmacol. Biol. Psychiatry     Publication Date:  2008 Feb 
Date Detail:
Created Date:  2008-02-05     Completed Date:  2008-05-30     Revised Date:  2014-09-19    
Medline Journal Info:
Nlm Unique ID:  8211617     Medline TA:  Prog Neuropsychopharmacol Biol Psychiatry     Country:  England    
Other Details:
Languages:  eng     Pagination:  315-31     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adult
Animals
Brain / physiology
Corpus Striatum / physiology
Depressive Disorder, Major / chemically induced,  epidemiology,  physiopathology
Disease Models, Animal
Hippocampus / physiology
Humans
Isotretinoin / adverse effects,  therapeutic use
Mice
Mood Disorders / chemically induced,  physiopathology*
Neurotransmitter Agents / physiology
Prefrontal Cortex / physiology
Retrospective Studies
Signal Transduction / physiology
Suicide / psychology,  statistics & numerical data
Tretinoin / adverse effects,  physiology*
Grant Support
ID/Acronym/Agency:
K24 MH076955/MH/NIMH NIH HHS; K24 MH076955-03/MH/NIMH NIH HHS; R01 HL088726/HL/NHLBI NIH HHS; R01 MH056120/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/Neurotransmitter Agents; 5688UTC01R/Tretinoin; EH28UP18IF/Isotretinoin
Comments/Corrections

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