Research Article| Volume 28, ISSUE 7, P569-587, October 01, 1990

Neuroendocrinological investigations during sleep deprivation in depression II. Longitudinal measurement of thyrotropin, TH, cortisol, prolactin, GH, and LH during sleep and sleep deprivation

  • Andreas Baumgartner
    Address reprint requests to Dr. A. Baumgartner, Psychiatrische Klinik und Poliklinik, Klinikum Rudolf-Virchow (Charlottenburg) der Freien Universität Berlin, Eschenalle 3, D-1000 Berlin 19, Federal Republic of Germany.
    From the Psychiatrische Klinik und Poliklinik, Klinikum Rudolf-Virchow (Charlottenburg) der Freien Universität Berlin, FRG
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  • Dieter Riemann
    Max Planck Institut für Psychiatrie in Munich, FRG
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  • Mathias Berger
    Max Planck Institut für Psychiatrie in Munich, FRG
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  • Author Footnotes
    ∗∗ D.R. is at the Zentralinstitut für Seelische Gesundheit, Mannheim, FRG
    ∗ M.B. is now at the Psychiatrische Klinik in Freiburg
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      Thyrotropin (TSH), thyroxin (T4), triiodothyronine (T3), free T3 (fT3), cortisol, prolactin, and human growth hormone (HGH) were measured every 2 hr during a night of sleep, the following day, and a night of sleep deprivation (SD) in 14 patients with major depressive disorder. In subgroups fT4 (n = 5), reverse T3 (rT3), and luteinizing hormone (LH) (n = 6) were also investigated. Significant increases in TSH, T4, fT4, T3, fT3, rT3, and cortisol and decreases in prolactin levels occurred during the night of SD, compared to the pattern during the night of sleep. The pre-SD T4 and T3 levels of the responders to SD were already higher than in the nonresponders, and increased less during SD. The cortisol and HGH concentrations of the responders rose higher during SD than those of the nonresponders. Changes in TSH and prolactin were not correlated to clinical response. Analysis of possible neurochemical mechanisms underlying this “pattern” of changes in different endocrine profiles suggests that enhanced noradrenergic activity might play a role in the changes in TSH, cortisol, thyroid hormones, and possibly HGH secretion during SD, and increased dopaminergic tone probably induced the decline in prolactin levels. Additional effects of the serotonergic system cannot be excluded at present. In conclusion, the data suggest that enhanced noradrenergic activity of the locus coeruleus stimulates alpha and/or beta adrenergic receptors in depressed patients during SD. This mechanism could well be involved in the antidepressant effect of this therapy.
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