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Review| Volume 20, ISSUE 7, P764-784, July 1985

Animal models of depression: Parallels and correlates to severe depression in humans

  • James A. Jesberger
    Footnotes
    Affiliations
    Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
    Search for articles by this author
  • J.Steven Richardson
    Correspondence
    Address reprint requests to Dr. J. Steven Richardson, Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
    Footnotes
    Affiliations
    Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada

    Department of Psychiatry, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
    Search for articles by this author
  • Author Footnotes
    1 The authors wish to thank Jackie Bitz and Margaret Matheson for secretarial assistance in preparing this manuscript.
DOI:https://doi.org/10.1016/0006-3223(85)90156-8
Animal models of depression: Parallels and correlates to severe depression in humans
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      Abstract

      Drugs with antidepressant properties in patients with severe depression also have various behavioral and neurochemical effects in animals. This has given rise to numerous animal models that have been suggested to be valid for research into the neurobiology of depression and the neurochemical mechanisms of the antidepressant drugs. However, considerable evidence from many avenues of research indicates that severe depression is a biochemical disorder that develops in those individuals with some predisposing neurochemical vulnerability. Although the predisposing biochemical abnormality has not been identified, it may be related to the neurochemical mechanisms that regulate impulse traffic in various neural systems and maintain the homeostatic balance of neural activity within the brain. Therefore, the appropriate animal model for severe depression should have some disruption of neural functioning that is returned to normal by the chronic administration of antidepressant drugs. Of the numerous animal models of depression that have been presented in the literature, only the rat with olfactory bulb lesions meets this requirement. The behavioral and endocrine abnormalities induced by the olfactory bulb lesions are reversed by chronic (but not acute) treatment with antidepressants of various classes. Of the existing animal models of severe depression, the olfactory bulbectomy model holds the most promise for elucidating the neurobiology of depression and the neurochemistry of antidepressant drugs.
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      Article info

      Publication history

      Received in revised form: December 26, 1984
      Received: October 13, 1984

      Identification

      DOI: https://doi.org/10.1016/0006-3223(85)90156-8

      Copyright

      © 1985 Published by Elsevier Inc.

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