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Rapid tryptophan depletion reverses phenelzine-induced suppression of REM sleep.

Author(s): Landolt HP, Kelsoe JR, Rapaport MH, Gillin JC

Affiliation(s): Department of Psychiatry, University of California at San Diego, VA San Diego Healthcare System, San Diego, CA, USA. landolt@pharma.unizh.ch

Publication date & source: 2003-03, J Sleep Res., 12(1):13-8.

Publication type: Clinical Trial; Randomized Controlled Trial; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.

Treatment with the monoamine oxidase inhibitor phenelzine completely suppressed rapid eye movement (REM) sleep in five depressed patients. Hypothesizing that increased serotonergic neurotransmission eliminated REM sleep, we administered a tryptophan-free amino acid drink (TFD) known to reduce plasma tryptophan and brain levels of serotonin. The TFD reversed the REM sleep suppression, while the control drink (TFD plus tryptophan) had virtually no effect on sleep. Neither TFD nor control drink affected mood, total sleep time, sleep efficiency or the all-night electroencephalogram power spectra in non-rapid eye movement (NREM) sleep. We report the first non-disruptive, double-blind method for studying human subjects overnight with and without REM sleep. It opens up a novel strategy for investigating the functions of REM sleep, and the roles of serotonin and REM sleep in the regulation of NREM sleep and mood.

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