Citation

Pandey GN, Dwivedi Y. Curr. Psychiatry Rev. 2006; 2(1): 51-75.

Copyright

(Copyright © 2006, Bentham Science Publishers)

DOI

10.2174/157340006775101436

PMID

unavailable

Abstract

Suicide is a major public concern and in the teenage population it is the third leading cause of death. Its neurobiology is not well-understood, but recent postmortem brain studies have provided greater understanding of the neurobiological abnormalities associated with suicide. Earlier postmortem brain studies focused on monoamine receptor subtypes, namely, serotonin, e.g., (5HT)1A, 5HT2A, and adrenergic receptors. Later, various components of the signaling cascades to which these receptors are linked were examined; 5HT2A or α1-adrenergic receptors are linked to the phosphoinositide (PI) signaling system, and β-adrenergic receptors are linked to the adenylyl cyclase (AC) system. These studies revealed abnormalities in the components of the signaling systems: G proteins, the effectors phospholipase C (PLC) and AC, or second and third messengers systems, such as protein kinase C (PKC) and protein kinase A (PKA). Further studies found that downstream transcription factors, such as cAMP-response-element-binding protein (CREB), were also affected. Here we critically review the studies, focusing primarily on monoamine receptors and the components of PI and AC signaling cascades in suicide, primarily in postmortem brain. These studies provide a better understanding of the pathophysiological abnormalities associated with suicide and may lead to new therapeutic agents targeting specific sites in the signaling cascade. © 2006 Bentham Science Publishers Ltd.

Language: en

Keywords

human; suicide; Suicide; autopsy; depression; aggression; schizophrenia; cause of death; suicide attempt; suicidal behavior; serotonin 1A receptor; risk factor; hopelessness; review; Mood disorders; antidepressant agent; neuroleptic agent; fenfluramine; pathophysiology; serotonin uptake inhibitor; priority journal; anxiety disorder; homovanillic acid; signal transduction; guanine nucleotide binding protein; Signal transduction; nonhuman; enzyme activation; serotoninergic system; messenger RNA; unindexed drug; atypical antipsychotic agent; drug response; protein expression; serotonin transporter; adrenergic system; lithium salt; protein function; serotonin 2A receptor; brain derived neurotrophic factor; drug targeting; adenylate cyclase; alpha 1 adrenergic receptor; alpha 2 adrenergic receptor; beta adrenergic receptor; brain derived neurotrophic factor receptor; cyclic AMP dependent protein kinase; cyclic AMP responsive element binding protein; glycogen synthase kinase 3beta; Kinases; MARCKS protein; Monoamine receptors; monoaminergic system; phosphatidylinositide; phospholipase A2; phospholipase C; protein kinase C alpha; protein kinase C beta; protein kinase C gamma; second messenger; serotonin 2C receptor; Transcription factors