Cytomorphometric changes in the dorsal raphe neurons after rapid eye movement sleep deprivation are mediated by noradrenalin in rats

Abstract

ObjectivesThis study was carried out to investigate the effect of rapid eye movement sleep (REMS) deprivation (REMSD) on the cytomorphology of the dorsal raphe (DR) neurons and to evaluate the possible role of REMSD-induced increased noradrenalin (NA) in mediating such effects.MethodsRats were REMS deprived by the flowerpot method; free moving normal home cage rats, large platform and post REMS-deprived recovered rats were used as controls. Further, to evaluate if the effects were induced by NA, separate sets of experimental rats were treated (i.p.) with α1-adrenoceptor antagonist, prazosin (PRZ). Histomorphometric analysis of DR neurons in stained brain sections were performed in experimental and control rats; neurons in inferior colliculus (IC) served as anatomical control.ResultsThe mean size of DR neurons was larger in REMSD group compared to controls, whereas, neurons in the recovered group of rats did not significantly differ than those in the control animals. Further, mean cell size in the post-REMSD PRZ-treated animals was comparable to those in the control groups. IC neurons were not affected by REMSD.ConclusionsREMS loss has been reported to impair several physiological, behavioral and cellular processes. The mean size of the DR neurons was larger in the REMS deprived group of rats than those in the control groups; however, in the REMS deprived and prazosin treated rats the size was comparable to the normal rats. These results showed that REMSD induced increase in DR neuronal size was mediated by NA acting on α1-adrenoceptor. The findings suggest that the sizes of DR neurons are sensitive to REMSD, which if not compensated could lead to neurodegeneration and associated disorders including memory loss and Alzheimer's disease.

Noradrenaline from Locus Coeruleus Neurons Acts on Pedunculo-Pontine Neurons to Prevent REM Sleep and Induces Its Loss-Associated Effects in Rats

“…The NA-induced effect, activation of the enzyme in the whole brain in this case, may be supported by the fact that the LC neurons have been reported to project throughout the brain (Samuels and Szabadi, 2008), and increased NA as well as TH mRNA have been reported in the rat brain after REMSD (Porkka-Heiskanen et al, 1995; Basheer et al, 1998). Also, it has been reported that in rat brains REMSD-induced changes in several enzyme activities (Thakkar and Mallick, 1991, 1993a,b; Amar and Mallick, 2015) and neuronal cytomorphology (Ranjan et al, 2010) are mediated by elevated level of NA.…”

Effect of REM sleep deprivation on the antioxidant status in the brain of wistar rats

“…Importance of REM sleep has been suggested by the study of Ranjan et al 29 who have concluded that REMSD could lead to neurodegeneration memory loss and Alzheimer’s disease. Sleep deprivation or prolonged wakefulness leads to decrements in cognitive performance, which is recognized as a major hazard to public safety and implicated in vehicular accidents, industrial catastrophes and other incidents involving error in human performance.…”

Rapid Eye Movement Sleep Deprivation Induces Neuronal Apoptosis by Noradrenaline Acting on Alpha1 Adrenoceptor and by Triggering Mitochondrial Intrinsic Pathway

“…Sleep has been divided into rapid eye movement sleep (REMS) and non-REMS, and as a common factor, at least the former is affected in most of the psychosomatic and neurodegenerative disorders. We have shown earlier that experimental REMS deprivation (REMSD) affects neuronal cytomorphology and structural protein leading to neuronal apoptosis and loss, and these effects were mediated by REMSD-associated elevation in the level of noradrenaline (NA) in the brain ( 1 – 3 ). Our contention gets supported by a recent report in humans that gray matter volume is reduced upon sleep disturbance ( 4 ).…”