AJP - Regulatory, Integrative and Comparative Physiology, Vol 268, Issue 6 1456-R1463, Copyright © 1995 by American Physiological Society
Noradrenergic activity in rat brain during rapid eye movement sleep deprivation and rebound sleep
T. Porkka-Heiskanen, S. E. Smith, T. Taira, J. H. Urban, J. E. Levine, F. W. Turek and D. Stenberg
Department of Physiology, University of Helsinki, Finland.
Noradrenergic locus ceruleus neurons are most active during waking and
least active during rapid eye movement (REM) sleep. We expected REM sleep
deprivation (REMSD) to increase norepinephrine utilization and activate the
tyrosine hydroxylase (TH) gene critical for norepinephrine 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 after 72 h of the platform
treatment. During the first 24 h, norepinephrine concentration, measured by
high-performance liquid chromatography/electrochemical detection, was lower
in the neocortex, hippocampus, and posterior hypothalamus in REMSD rats
than in large-platform controls. After 72 h of REMSD, TH mRNA, measured by
in situ hybridization, was increased in the locus ceruleus and
norepinephrine concentrations were increased. Polygraphy showed that
small-platform treatment caused effective and selective REMSD. Serum
corticosterone measurement by radioimmunoassay indicated that the
differences found in norepinephrine and TH mRNA were not due to differences
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.
