GROWTH HORMONE-RELEASING HORMONE (GHRH)-INDUCED EFFECTS ON SLEEP EEG AND NOCTURNAL SECRETION OF GROWTH-HORMONE, CORTISOL AND ACTH IN PATIENTS WITH MAJOR DEPRESSION

Studies in normal subjects and animals suggest that the neuropeptide g rowth hormone-releasing hormone (GHRH) is a common regulator of the sl eep EEG and nocturnal hormone secretion. In healthy volunteers GHRH pr ompts an increase in the amount of slow wave sleep (SWS) and in growth hormone (GH) secretion and blunting of cortisol release. Inhibition o f GHRH may contribute to sleep-endocrine aberrances during depression. We testes the effects of pulsatile application of 4 x 50 mu g GHRH on the sleep EEG and simultaneously investigated nocturnal hormone secre tion in 10 inpatients (four females, six males) with the acute episode of major depression. In contrast to the effects of placebo, GH secret ion in creased distinctly and rapid-eye-movement (REM) density decreas ed during the second half of night. No other significant changes in sl eep-endocrine activity, including SWS, cortisol and ACTH secretion, co uld be observed. We assume that hypothalamic-pituitary-adrenocortical system activity and slow wave sleep are inert to the influence of GHRH during acute depression. Cortisol and ACTH remained unchanged even in a subsample of five younger (aged 19-28 years) patients. This observa tion is in contrast to our recent finding that cortisol secretion is b lunted in young normal volunteers after GHRH. But on the other hand, G HRH is capable of stimulating GH and inducing a decrease in REM densit y in these subjects.