Noradrenergic function in suicide.
Although abnormalities in serotonergic function have been the major focus of studies on suicidal behavior, several studies indicate that abnormalities of noradrenergic function may also be involved in the pathophysiology of suicide. In this paper, we have reviewed some of the noradrenergic studies in suicide, including studies of the biosynthetic enzyme for norepinephrine, tyrosine hydroxylase (TH), the receptors for norepinephrine, alpha- and beta-adrenergic receptors, as well as the signaling cascades linked to beta-adrenergic receptors. In general, these studies indicate that the protein expression of TH, as well as alpha2- and beta2-adrenergic receptors, is increased in the postmortem brain of suicide victims. More studies are needed in order to examine extensively the role of noradrenergic function in suicidal behavior.
Pandey
Ghanshyam N
GN
The Psychiatric Institute, Department of Psychiatry, University of Illinois at Chicago 60612, USA. Gnpandey@psych.uic.edu
Dwivedi
Yogesh
Y
D006801:Humans; D008734:Methoxyhydroxyphenylglycol / Q000378:metabolism; D009638:Norepinephrine / Q000502:physiology*; D011493:Protein Kinase C / Q000502:physiology; D011941:Receptors, Adrenergic / Q000502:physiology; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D013405:Suicide / Q000523:psychology*; D014446:Tyrosine 3-Monooxygenase / Q000502:physiology
D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D008734:Methoxyhydroxyphenylglycol; D014446:Tyrosine 3-Monooxygenase; D011493:Protein Kinase C; D009638:Norepinephrine