Citation

González-Maeso J, Meana JJ. Curr. Neuropharmacol. 2006; 4(2): 127-138.

Copyright

(Copyright © 2006, Bentham Science Publishers)

DOI

10.2174/157015906776359586

PMID

unavailable

Abstract

Mood disorders such as major depression and bipolar disorder are common, severe, chronic and often life-threatening illnesses. Suicide is estimated to be the cause of death in up to approximately 10-15% of individuals with mood disorders. Alterations in the signal transduction through G protein-coupled receptor (GPCR) pathways have been reported in the etiopathology of mood disorders and the suicidal behavior. In this regard, the implication of certain GPCR subtypes such as α2A-adrenoceptor has been repeatedly described using different approaches. However, several discrepancies have been recently reported in density and functional status of the heterotrimeric G proteins both in major depression and bipolar disorder. A compilation of the most relevant research topics about the implication of heterotrimeric G proteins in the etiology of mood disorders (i.e., animal models of mood disorders, studies in peripheral tissue of depressive patients, and studies in postmortem human brain of suicide victims with mood disorders) will provide a broad perspective of this potential therapeutic target field. Proposed causes of the discrepancies reported at the level of G proteins in postmortem human brain of suicide victims will be discussed. © 2006 Bentham Science Publishers Ltd.

Language: en

Keywords

human; Suicide; autopsy; bipolar disorder; Bipolar disorder; cause of death; major depression; lithium; suicidal behavior; disease severity; serotonin 1A receptor; mood disorder; pathogenesis; Major depression; review; Mood disorders; serotonin; antidepressant agent; amitriptyline; clomipramine; desipramine; fluoxetine; imipramine; noradrenalin; electroconvulsive therapy; signal transduction; tranylcypromine; nonhuman; medical research; hypomania; neurobiology; histopathology; reserpine; disease model; protein function; drug targeting; alpha 2A adrenergic receptor; clorgyline; G protein coupled receptor; G protein-coupled receptors (GPCR); Heterotrimeric G proteins; heterotrimeric guanine nucleotide binding protein; iprindole; iproniazid; molecular mechanics; α 2-adrenoceptors