Abstract

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 sucide, including studies of the biosynthetic enzyme for norepinephrine, tyrosine hydroxylase (TH), the receptors for norepinephrine, α- and β-adrenergic receptors, as well as the signaling cascades linked to β-adrenergic receptors. In general, these studies indicate that the protein expression of TH, as well as α2- and β2-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.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call