Advertisement

α2-Adrenoceptor responsivity in depression: effect of chronic treatment with moclobemide, a selective MAO-A-inhibitor, versus maprotiline

  • K. P. Lesch
  • G. Laux
  • T. Mueller
Conference paper
Part of the Journal of Neural Transmission book series (NEURAL SUPPL, volume 32)

Summary

The effect of chronic treatment with the selective and reversible MAO-A-inhibitor moclobemide (MOC) vs. the norepinephrine reuptake inhibitor maprotiline (MAP) on α2-adrenoceptor responsivity was studied by clonidine (CLON)-evoked growth hormone (GH) release in major depressive disorder. Compared to matched controls the depressed patients showed attenuated CLON-induced GH responses before treatment with MOC or MAP. Chronic treatment with both MOC and MAP significantly improved the depressive symptomatology. Although a trend toward increased GH responses to CLON was demonstrated after treatment in both groups, neither MOC nor MAP had a complete effect on restoration of α2-adrenoceptor responsivity. No difference in insulin-like growth factor I (IGF-I) plasma concentrations before and after treatment with MOC or MAP was found. Our results support the view that antidepressants with different mechanisms of action may be capable of restoring α2-adrenoceptor function during recovery from a major depressive episode.

Keywords

Growth Hormone Depressed Patient Major Depressive Disorder Depressive Symptomatology Growth Hormone Response 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Charney DS, Heninger GR, Sternberg DE (1982) Failure of chronic antidepressant treatment to alter growth hormone response to clonidine. Psychiatry Res 7:135–138.PubMedCrossRefGoogle Scholar
  2. Checkley SA, Stade AP, Shur E, Dawling S (1981) A pilot study of the mechanism of action of desipramine. Br J Psychiatry 138:248–251.PubMedCrossRefGoogle Scholar
  3. Erb A, Laux G, Lesch KP (1988) Effects of moclobemide and maprotiline on hypothalamic-pituitary-somatotropic (HPS) axis function in depression. Psychopharmacology 96 [Suppl]: 279.Google Scholar
  4. Lesch KP, Laux G, Erb A, Pfueller H, Beckmann H (1988) Growth hormone (GH) response to GH-releasing hormone in depression: correlation with GH release following clonidine. Psychiatry Res 25:301–310.PubMedCrossRefGoogle Scholar
  5. Lesch KP, Rupprecht R (1989) Psychoneuroendocrine research in depression. II. Hormonal responses to releasing hormones as a probe for hypothalamicpituitary-endorgan dysfunction. J Neural Transm 75:179–194.Google Scholar
  6. Lesch KP, Mayer S, Disselkamp-Tietze J, Hoh A, Wiesmann M, Osterheider M, Schulte HM (1990) 5-HT1A receptor responsivity in unipolar depression: evaluation of ipsapirone-induced ACTH and cortisol secretion in patients and controls. Biol Psychiatry (in press).Google Scholar
  7. Lesch KP, Beckmann H (1990) Zur Serotonin-Hypothese der Depression. Fortschr Neurol Psychiat (in press).Google Scholar
  8. Matussek N, Ackenheil M, Hippius H, Mueller F, Schroeder HS, Schultes A, Wasilewski B (1980) Effect of clonidine on growth hormone release in psychiatric patients and controls. Psychiatry Res 2:25–36.PubMedCrossRefGoogle Scholar
  9. Siever LJ, Uhde TW, Insel TR, Roy BF, Murphy DL (1982) Growth hormone response to clonidine unchanged by chronic clorgyline treatment. Psychiatry Res 7:139–144.PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag 1990

Authors and Affiliations

  • K. P. Lesch
    • 1
    • 2
  • G. Laux
    • 1
  • T. Mueller
    • 1
  1. 1.Department of PsychiatryUniversity of WürzburgFederal Republic of Germany
  2. 2.Laboratory of Clinical Science NIMHNIH Clinical CenterBethesdaUSA

Personalised recommendations