Pharmacopsychiatry 2002; 35(4): 127-134
DOI: 10.1055/s-2002-33197
Original Paper
© Georg Thieme Verlag Stuttgart · New York

Relationship between Cortisol and Serotonin Metabolites and Transporters in Alcolholism

A. Heinz1, 4 , D. W. Jones1 , G. Bissette3 , D. Hommer2 , P. Ragan2 , M. Knable1 , S. Wellek4 , M. Linnoila2 , D. R. Weinberger1
  • 1Clinical Brain Disorders Branch, Intramural Research Program, NIMH, Bethesda, MD, USA
  • 2Laboratory of Clinical Studies, Intramural Research Program, NIAAA, Bethesda, MD, USA
  • 3Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson, MI, USA
  • 4Central Institute of Mental Health, University of Heidelberg, Mannheim, Germany
Supported in part by the Deutsche Forschungsgemeinschaft (Az: He 2597/1 - 1)Dr. Linnoila died in February 1998.Parts of this manuscript were orally presented by Dr. Heinz at the 30th Annual Meeting of the Society for Neuroscience in New Orleans, November 6th, 2000.
Further Information

Publication History

Manuscript received: 3. 1. 2001 Revised: 5. 12. 2001

Accepted: 20. 12. 2001

Publication Date:
06 August 2002 (online)

Background: Stress hormone activation may induce clinical depression via an interference with central serotonergic neurotransmission. In alcoholics, a reduction in serotonin transporters was associated with clinical depression, and an activation of cortisol secretion is frequently found during detoxification. We assessed the interaction between stress hormone activation, serotonin transporters, monoamine metabolites in the cerebrospinal fluid (CSF), and mood states in male and female alcoholics and healthy control subjects. Methods: The availability of serotonin transporters was measured with [I-123]β-CIT and SPECT in the raphe area of the brainstem in 31 alcoholics after four weeks of abstinence and in 25 age-matched healthy volunteers. Concentrations of plasma cortisol were measured on the day of the SPECT scan. Within one week after the SPECT scan, we assessed monoamine metabolites and corticotropin-releasing factor (CRF) in the CSF. Results: Clinical depression was associated with a reduction in serotonin transporter availability among male alcoholics. Among male alcoholics and healthy volunteers, CSF 5-HIAA and plasma cortisol concentrations were inversely correlated with the availability of raphe serotonin transporters and positively correlated with the severity of clinical depression. No significant correlations were observed between raphe serotonin transporters and HVA, MHPG and CRF concentrations in the CSF. Conclusion: Our findings support the hypothesis of an interaction between reduced serotonin transporters, stress hormone activation and clinical depression. They confirm the hypothesis that serotonergic neurotransmission dysfunction in alcoholism is limited to male alcoholics. The observed interactions between high cortisol concentrations and reduced serotonin transporter availability warrant further studies in major depression and other neuropsychiatric diseases with implied cortisol activation and serotonergic dysfunction.

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Andreas Heinz,MD 

Director and Chair, Dept. of Psychiatry of the Charité

Schumannstr. 20/21

10117 Berlin

Germany

Phone: +49 (30) 450 51 70 01

Fax: +49 (30) 450 51 79 10

Email: andreas.heinz@charite.de

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