Differential Neuroendocrine Responses to Thyrotropin-Releasing Hormone during Rapid Eye Movement and Slow Wave Sleep in Man*

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Abstract
The evidence that both TRH and somatostatin (SRIF) control TSH secretion prompted this study of the hypothesis that slow wave sleep (SWS)-induced GH secretion may be related to a decrease in hypothalamic SRIF release. Ten adult men spent 1 accommodation night, followed by 2 experimental nights, in the sleep laboratory, during which electroencephalogram monitoring and blood sampling by iv catheter were performed. Subjects received TRH (50µg, iv) in 0.5 ml saline or saline alone during SWS and rapid eye movement sleep (REM) on 1 night and a reversed injection protocol on the other night. Each subject received only one TRH injection per night, during either SWS or REM. Blood was sampled every 30 min during sleep (lights off from 2300–0700 h), except immediately after each injection, when samples were taken at 0, 5, 10, 15, 30, 45, 60, 90, and 120 min. Serum TSH, GH, PRL, and cortisol levels were determined by RIA. Characteristic sleep patterns of GH and cortisol secretion were observed in these subjects, with no differences between the 2 experimental nights. The mean GH level during SWS (3.7 ± 1.2 ng/ml) was significantly higher than that during REM sleep (0.7±0.2 ng/ml). Infusion of saline alone had no effect on any of the hormones. TRH infusion had no effect on serum GH or cortisol levels, but it significantly increased serum TSH and PRL over baseline control levels during both SWS and REM sleep. Whereas PRL was equally elevated over baseline by TRH during both SWS (70.1±5.5 ng/ml) and REM (68.3±6.2 ng/ml), the TSH response was significantly higher during SWS (33.9±6.1 µU/ml) than during REM (20.3±3.2µU/ml). The greater response of TSH to TRH during SWS (↑GH) than during REM (↓GH) supports the hypothesis that SWS–induced GH release is related to a decrease in endogenous hypothalamic SRIF levels and provides further evidence for the dual hypothalamic control of TSH.