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State and trait abnormalities in serotonin function in major depression.

Zubin Bhagwagar1, Richard Whale, Philip J Cowen

  • 1University Department of Psychiatry, Warneford Hospital, Oxford OX3 7JX, UK.

The British Journal of Psychiatry : the Journal of Mental Science
|January 5, 2002
PubMed
Summary
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Impaired serotonin function in depression may persist after recovery, as indicated by blunted prolactin responses to citalopram. Cortisol response recovery suggests resolution of hypothalamic-pituitary-adrenal axis dysfunction.

Area of Science:

  • Neuroendocrinology
  • Psychiatry
  • Pharmacology

Background:

  • Depression is often linked to impaired brain serotonin (5-HT) function.
  • It remains debated whether this impairment resolves with clinical recovery from depression.

Purpose of the Study:

  • To investigate brain 5-HT function in depression using endocrine responses to citalopram.
  • To compare acute depression, recovered depression, and healthy controls.

Main Methods:

  • Double-blind, placebo-controlled study.
  • Measured prolactin and cortisol responses to intravenous citalopram (10 mg).
  • Included acutely depressed patients, unmedicated recovered patients, and healthy controls.

Main Results:

Related Experiment Videos

  • Prolactin responses to citalopram were blunted in both acutely depressed and recovered subjects.
  • Cortisol responses were blunted in acutely depressed patients but normalized in recovered subjects.

    • Conclusions:

    • Impaired 5-HT neurotransmission may serve as a trait marker for depression vulnerability.
    • Recovery of cortisol response indicates resolution of hypothalamic-pituitary-adrenal axis dysfunction in depression.