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A Review

WILLIAM E. BUNNEY, JR., MD; JOHN M. DAVIS, MD

Arch Gen Psychiatry. 1965;13(6):483-494.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

LITTLE IS known about the possible etiological biochemical factors relating to depressive reactions. Clinical evidence suggests that many depressions respond to the following somatic treatment: electric convulsive therapy (ECT), the imipramine type of drugs, and the monoamine oxidase inhibitor group of drugs.^2,3 Do these two classes of drugs have common factors in their mechanism of action and can this be related to the fact that one antihypertensive agent, namely, reserpine, produces severe depression in a small but consistent number of hypertensive patients?^4-8

Rosenblatt et al,⁹ in 1959, were among the first to specifically suggest that changes in brain norepinephrine (NEP) may be involved in depression. Based in part on the knowledge of the effect of reserpine and monoamine oxidase inhibitors on depressed mood and norepinephrine (NEP), they hypothesized that the depressive state might be associated with a relative decrease of norepinephrine . . . [Full Text PDF of this Article]

Author Affiliations
BETHESDA, MD

From the Psychosomatic Section, Adult Psychiatry Branch, National Institute of Mental Health.

Footnotes
Submitted for publication May 19, 1965.

Reprint requests to National Institute of Mental Health, Adult Psychiatry Branch, Bethesda, Md 20014 (Dr. Bunney).

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