ArticleBehavioral and brain functions : BBF2010
Cytomorphometric changes in the dorsal raphe neurons after rapid eye movement sleep deprivation are mediated by noradrenalin in rats.
Article in Behavioral and brain functions : BBF, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 33 citations in OpenAlex.
- 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.Neuroprotection (Chichester, England) · 2025Article
- Review
- Curcumin mitigates the sleep-deprivation impacts on rat hypothalamic paraventricular nucleus.IBRO neuroscience reports · 2023Article
- Neurogenesis in the rat neonate's hippocampus with maternal short-term REM sleep deprivation restores by royal jelly treatment.Brain and behavior · 2021Article
- Curcumin prevents neuronal loss and structural changes in the superior cervical (sympathetic) ganglion induced by chronic sleep deprivation, in the rat model.Biological research · 2020Article
- Effects of Sleep Deprivation on the Tryptophan Metabolism.International journal of tryptophan research : IJTR · 2020Review
- Noradrenaline Acting on Alpha1 Adrenoceptor as well as by Chelating Iron Reduces Oxidative Burden on the Brain: Implications With Rapid Eye Movement Sleep.Frontiers in molecular neuroscience · 2019Article
- Relevance of deprivation studies in understanding rapid eye movement sleep.Nature and science of sleep · 2018Review
- Rapid Eye Movement Sleep Deprivation Induces Neuronal Apoptosis by Noradrenaline Acting on Alpha1 Adrenoceptor and by Triggering Mitochondrial Intrinsic Pathway.Frontiers in neurology · 2016Article
- Wake-active neurons across aging and neurodegeneration: a potential role for sleep disturbances in promoting disease.SpringerPlus · 2015Article
- Cytomorphometric Changes in Hippocampal CA1 Neurons Exposed to Simulated Microgravity Using Rats as Model.Frontiers in neurology · 2014Article
- A hypnic hypothesis of Alzheimer's disease.Neuro-degenerative diseases · 2013Review
- Effect of REM sleep deprivation on the antioxidant status in the brain of Wistar rats.Annals of neurosciences · 2012Article
- Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation.Basic and clinical neuroscienceReview
- Article
- Targeting modulation of noradrenalin release in the brain for amelioration of REMS loss-associated effects.Journal of translational internal medicineReview
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.