Noradrenergic activity in rat brain during rapid eye movement sleep deprivation and rebound sleep

HOME PAGE


Am J Physiol Regul Integr Comp Physiol 268: R1456-R1463, 1995; 0363-6119/95 $5.00

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.

Norepinephrine
From Wikipedia, the free encyclopedia

Noradrenaline (BAN) (abbreviated NA or NAd) or norepinephrine (INN) (abbreviated norepi or NE) is a catecholamine with dual roles as a hormone and a neurotransmitter.[2]
As a stress hormone, norepinephrine affects parts of the brain where attention and responding actions are controlled. Along with epinephrine, norepinephrine also underlies the fight-or-flight response, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle.
However, when norepinephrine acts as a drug it will increase blood pressure by its prominent increasing effects on the vascular tone from α-adrenergic receptor activation. The resulting increase in vascular resistance triggers a compensatory reflex that overcomes its direct stimulatory effects on the heart, called the baroreceptor reflex, which results in a drop in heart rate called reflex bradycardia.
Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase.[3] It is released from the adrenal medulla into the blood as a hormone, and is also a neurotransmitter in the central nervous system and sympathetic nervous system where it is released from noradrenergic neurons. The actions of norepinephrine are carried out via the binding to adrenergic receptors.

Mechanism
Norepinephrine is synthesized from tyrosine as a precursor, and packed into synaptic vesicles. It performs its action by being released into the synaptic cleft, where it acts on adrenergic receptors, followed by the signal termination, either by degradation of norepinephrine, or by uptake by surrounding cells.

http://en.wikipedia.org/wiki/Norepinephrine