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An evaluation of the role of the noradrenergic system in the neurobiology of depression: a review
Author(s) -
Redmond Anna M.,
Leonard Brian E.
Publication year - 1997
Publication title -
human psychopharmacology: clinical and experimental
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.461
H-Index - 78
eISSN - 1099-1077
pISSN - 0885-6222
DOI - 10.1002/(sici)1099-1077(199709/10)12:5<407::aid-hup918>3.0.co;2-1
Subject(s) - tyrosine hydroxylase , monoamine neurotransmitter , receptor , antidepressant , mechanism of action , dopamine , endocrinology , norepinephrine , medicine , neurotransmitter , glutamate receptor , depression (economics) , psychology , neuroscience , serotonin , biology , in vitro , hippocampus , biochemistry , macroeconomics , economics
With increased understanding of the neurobiology of depression, the role of the noradrenergic system is achieving greater significance. Unfortunately, the exact role of noradrenaline in depressive disorders is difficult to determine due to contradictory and inconsistent results from metabolite (MHPG) and receptor (α‐ and β‐adrenoceptors) binding studies which appear to be due to differences in experimental methods and variations between the age of tissue samples and the patient groups being studied. The role of tyrosine hydroxylase, the rate‐limiting enzyme in the synthesis of noradrenaline has only recently been explored. A downregulation of tyrosine hydroxylase mRNA expression seems to be a common mechanism of action of antidepressant treatments and indicates that the site of action of antidepressants may occur at the level of gene expression. Evidence suggests that corticotrophin releasing factor (CRF) may regulate tyrosine hydroxylase activity and so may provide a link between the monoamine and endocrine theories of depression. Glutamate and sigma receptors have also been implicated in having a role to play in affective disorders and will be discussed in this review as these receptors may be indirectly involved in modulating the activity of the noradrenergic system. © 1997 John Wiley & Sons, Ltd.