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Aromatase changes in depression: A postmortem and animal experimental study.

Juan-Li Wu1, Yang He1, Radovan Hrubý2

  • 1Department of Neurobiology, Key Laboratory of Medical Neurobiology of Ministry of Health of China, Zhejiang Province Key Laboratory of Neurobiology, Zhejiang Province Key Laboratory of Mental Disorder's Management, Zhejiang University School of Medicine, Hangzhou, China.

Psychoneuroendocrinology
|December 27, 2016
PubMed
Summary

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Depression may not involve increased aromatase, an enzyme converting androgens to estrogens. Studies found lower aromatase in depressed patients and no effect of an aromatase inhibitor on depression-like behaviors in rats.

Area of Science:

  • Neuroendocrinology
  • Molecular Psychiatry
  • Behavioral Neuroscience

Background:

  • Hyperactive hypothalamo-pituitary-adrenal (HPA) axis is characteristic of depression.
  • Androgens inhibit HPA activity, while estrogens stimulate it.
  • Aromatase facilitates androgen-to-estrogen conversion.

Purpose of the Study:

  • Investigate aromatase levels in human postmortem hypothalamus of major depressive disorder (MDD) patients.
  • Examine the effect of an aromatase inhibitor on depression-like symptoms in a rat model.

Main Methods:

  • Quantified aromatase immunoreactivity in the paraventricular nucleus (PVN) of MDD patients and controls.
  • Administered 1,4,6-androstatriene-3,17-dione (ATD), an aromatase inhibitor, to chronic unpredictable mild stress (CUMS) rats.
Keywords:
1,4,6-Androstatriene-3,17-dioneAromataseChronic unpredictable mild stressDepressionParaventricular nucleus

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  • Measured testosterone and corticosterone levels and depression-like behaviors.

    • Main Results:

    • MDD patients showed significantly decreased PVN aromatase immunoreactivity compared to controls.
    • ATD administration increased testosterone levels in rats but did not significantly alter depression-like behaviors or corticosterone levels.

    Conclusions:

    • Adult alterations in aromatase do not appear to be a major factor in the pathogenesis of depression symptoms.
    • Findings suggest complex regulatory mechanisms of the HPA axis in depression.