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Antidepressant Effect of Thyrotropin‐Releasing Hormone (TRH) and the Plasma Thyrotropin Levels in Depression
Author(s) -
Takahashi Saburo,
Kondo Hisao,
Yoshimura Manabu,
Ochi Yukio
Publication year - 1973
Publication title -
psychiatry and clinical neurosciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.609
H-Index - 74
eISSN - 1440-1819
pISSN - 1323-1316
DOI - 10.1111/j.1440-1819.1973.tb02663.x
Subject(s) - thyrotropin releasing hormone , medicine , endocrinology , neuroticism , euthyroid , depression (economics) , trh stimulation test , antidepressant , hormone , hypothalamic–pituitary–thyroid axis , psychology , imipramine , psychotic depression , psychiatry , thyroid hormones , psychosis , social psychology , alternative medicine , personality , pathology , hippocampus , economics , macroeconomics
SUMMARY Twenty‐four patients with mental depression received thyrotropin‐releasing hormone (TSH). 14 patients in Group A were treated with a series of TRH injections 500 μ g three times a week, for two to three weeks, and 150 mg/day of imipramine administration in a cross‐over comparison. Only three patients showed mild improvement in their depressive symptoms, while imipramine, which was administered in place of TRH, revealed to have more effect on their depression. Antidepressant effect of TRH can be evaluated as not exceeding that of the tricyclics. A single dose of 500 μ g TRH in Group B, consisting of 10 depressed inpa‐tients, caused neither subjective feelings of improvement nor behavioral changes. Twenty‐five percent of depressed patients showed an inadequate TSH response to TRH injection, although all the patients were euthyroid in their thyroid function tests. Three of four neurotic‐depressives, with pro longed mental symptoms of several years, revealed a distinctly diminished plasma TSH response to TRH injection. These findings suggest an abnormality in the hypothalamic‐pituitary axis, which may cause the fixation of mental symptoms. Neurotic‐depressive symptomatology protracted for many years may be based on an unknown neuroendocrine dysfunctions. The implications of these findings remain to be explored.