Noradrenergic activity in the rat brain during rem sleep deprivation and rebound sleep. Porkka-Heiskanen, Tarja, Sabrina E. Smith, Tomi Taira, Janice H. Urban, Jon E. Levine, Fred W. Turek, and Dag Stenberg. Department of Physiology, P.O.Box 9, SF-00014 University of Helsinki, Finland and Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208 (USA), Current address: New York University School of Medicine, 550 First Avenue, New York, NY 10016
APStracts 2:0009R, 1995.
Noradrenergic locus coeruleus neurons are most active during waking, and least active during REM sleep. We expected REM sleep deprivation (REMSD) to increase noradrenaline (NA) utilization, and activate the tyrosine hydroxylase (TH) gene, critical for NA production. Male Wistar rats were deprived of REM sleep with the platform method. Rats were decapitated after 8, 24 or 72 h on small (REMSD) or large (control) platforms, or after 8 or 24 h of rebound sleep following 72 h of the platform treatment. During the first 24 h, NA concentration measured by HPLC/EC was lower after REMSD than in large platform controls in neocortex, hippocampus, and posterior hypothalamus. After 72 h of REMSD, TH mRNA measured by in situ hybridization was increased in the LC, and NA concentrations were increased. Polygraphy showed that small platform treatment caused effective and selective REMSD. Serum corticosterone measurement by RIA indicated that the differences found in NA and TH mRNA were not due to difference in stress between the treatments. The novel finding of sleep deprivation-specific increase in TH gene expression indicates an important mechanism of adjusting to sleep deprivation. 

Received 16 August 1994; accepted in final form 9 January 1995
APS Manuscript Number R455-4.
Article publication pending Am. J. Physiol. (Regulatory Integrative Comp.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 February 1995.