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Noradrenergic Function and Depression, Too Much or Too Little?

Published online by Cambridge University Press:  18 September 2015

J.W. Maas  and
Y. Huang
J.W. Maas*
Affiliation:
Department of Psychiatry, School of Medicine, Yale University, New Haven, Connecticut
Y. Huang
Affiliation:
Department of Psychiatry, School of Medicine, Yale University, New Haven, Connecticut
*
Dept. of Psychiatry, School of Medicine, Yale University, New Haven, Connecticut, U.S.A. 06516
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Summary:

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Antithetical hypotheses as to CNS noradrenergic function in depressed patients can be constructed from results of pharmacological studies of the effects of antidepressant drugs. The experimental data supporting each of these opposing propositions is briefly reviewed in this paper. Finally, the results of clinical studies of noradrenergic function in depressed patients are noted and discussed in terms of these disparate hypotheses.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 7 , Issue 3 , August 1980 , pp. 267 - 268
Copyright
Copyright © Canadian Neurological Sciences Federation 1980

References

REFERENCES

Burney, W.E Jr., Davis, J.M. (1965). Norepinephrine in depressive reactions. Arch Gen Psychiatry 13: 483–494.Google Scholar
Banjerjee, S.P., Kung, L.S., Riggi, J.S., Chanda, S.K., (1977). Development of β-adrenergic receptor subsensitivity by antidepressants. Nature (London) 268: 455–456.CrossRefGoogle Scholar
Cobbin, D.M., Requin-Blow, B., Williams, L.R., et al. (1979). Urinary MHPG levels and tricyclic antidepressant drug selection. Arch Gen Psychiatry 36: 1111–1118CrossRefGoogle ScholarPubMed
Crews, F.T., Smith, C.B. (1978). Presynaptic Alpha-receptor subsensitivity after long-term antidepressant treatment. Science 202: 322–324.CrossRefGoogle ScholarPubMed
Huang, Y. (1979). Chronic desipramine treatment increases activity of noradrenergic postsynaptic cells. Life Sci 25–11: 709–716.CrossRefGoogle ScholarPubMed
Maas, J.W. (1978). Clinical and biochemical heterogeneity of depressive disorders. Annals of Int Medicine 88: 556–563.CrossRefGoogle ScholarPubMed
Schildkraut, J. (1965). The catecholamine hypothesis of affective disorders: A review of supporting evidence. Am J Psychiatry 122: 508–522.CrossRefGoogle ScholarPubMed
Schildkraut, J.J., Winokur, A., Applegate, C.W. (1970). Norepinephrine turnover and metabolism in rat brain after long-term administration of imipramine. Science 1168: 867–869.CrossRefGoogle Scholar
Segal, D.S., Kuczenski, R., Mandell, A.J. (1974). Theoretical implications of drug-induced adaptive regulation for a biogenic amine hypothesis of affective disorder. Biol Psychiatry 9: 147–159.Google ScholarPubMed
Sulser, F., Vetulani, J., Mobley, P.L. (1978). Commentary: mode of action of antidepressant drugs. Biochem Pharmacol. 27: 257–261.CrossRefGoogle Scholar
Svensson, T.H., Usdin, T. (1978). Feedback inhibition of brain noradrenaline neurons by tricyclic antidepressants: Alpha-receptor mediation. Science 202: 1089–1091.CrossRefGoogle ScholarPubMed
Taylor, K.M., Randall, P.K. (1975). Depletion of S-adenosl-methionine in mouse brain by antidepressive drugs. J. Pharmacol. Exp. Ther. 194: 301–310.Google ScholarPubMed
Van Kammen, D.P., Murphy, D.G. (1978). Prediction of antidepressant response by a one-day d-amphetamine trial. Amer J Psychiatry 135: 1179–1184.Google ScholarPubMed
Wolfe, B.B., Harden, T.K., Sporn, J.R., Molinoff, P.B. (1978). Presynaptic modulation of beta adrenergic receptors in rat cerebral cortex after treatment with antidepressants. J. Pharmacol. Exp. Ther. 207: 446–457.Google ScholarPubMed