Rapid eye movement sleep deprivation induced gene regulation for modulation of noradrenaline level in brain regions of rats: Implications with chronic sleep-loss associated pathophysiological conditions.

Background: Rapid eye movement sleep (REMS) loss affects almost all physiological processes, while it itself is affected in disorders. REMS maintains optimum level of noradrenaline (NA) in a healthy individual, while increased NA during disturbed REMS is associated with diseases. The synthesis, release, and degradation of neurotransmitter are modulated by biomolecules, which are genetically encoded. The aim of this study is to understand the transcriptional and translational changes of those biomolecules in locus coeruleus (LC) and pedunculo-pontine tegmentum (PPT) in association with REMS and its loss, which is expected to help us explain associated acute and chronic pathophysiological changes. Methods: In this study, male inbred Wistar rats were deprived of REMS for 96 h using classical flowerpot method; free-moving-, large platform- and recovery-control sets were also conducted ( Results: Upon rapid eye movement sleep deprivation (REMSD), although TH and DBH protein expressions altered significantly in all the brain areas, the latter was highest in LC (F Conclusion: The differential expressions of the genes and corresponding proteins (enzymes) responsible for synthesis and degradation of NA support sustained increase in NA upon REMSD that explains underlying causes of REMSD associated chronic effects, which may be exploited for amelioration of REMSD-associated disorders.