Abstract
Results from preliminary clinical reports have indicated that thyrotropin-releasing hormone (TRH) produces improvement in depressed patients. In the present study, doses of TRH at least 25 times greater than those reported as clinically effective on a mg/kg basis were evaluated for antidepressant activity in the conscious dog. Clinically effective antidepressants, such as MAO inhibitors and tricyclics like imipramine, potentiate certain behavioral, autonomic, and cardiovascular responses produced by the indole alkaloid yohimbine, whereas general CNS stimulants such as amphetamine or cocaine do not potentiate these responses. Both 50 and 100 ug/kg doses of TRH failed to potentiate yohimbine effects. Certain gross similarities in effects produced by TRH and amphetamine observed in this study support the view that beneficial effects of TRH in depression may be related to general sympathetic activation produced by this hormone.
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