Abstract
Sleep disorders are associated with cognitive impairment. Selective rapid eye movement sleep (REMS) deprivation (REMSD) alters several physiological processes and behaviors. By employing NGS platform we carried out transcriptomic analysis in brain samples of control rats and those exposed to REMSD. The expression of genes involved in chromatin assembly, methylation, learning, memory, regulation of synaptic transmission, neuronal plasticity and neurohypophysial hormone synthesis were altered. Increased transcription of BMP4, DBH and ATP1B2 genes after REMSD supports our earlier findings and hypothesis. Alteration in the transcripts encoding histone subtypes and important players in chromatin remodeling was observed. The mRNAs which transcribe neurotransmitters such as OXT, AVP, PMCH and LNPEP and two small non-coding RNAs, namely RMRP and BC1 were down regulated. At least some of these changes are likely to regulate REMS and may participate in the consequences of REMS loss. Thus, the findings of this study have identified key epigenetic regulators and neuronal plasticity genes associated to REMS and its loss. This analysis provides a background and opens up avenues for unraveling their specific roles in the complex behavioral network particularly in relation to sustained REMS-loss associated changes.
Highlights
Sleep is amongst the most conserved instinctive behaviors
It has been consistently shown that the synaptosomal Na–K ATPase activity is increased after rapid eye movement sleep deprivation (REMSD) in rats
This was further confirmed by Quantitative Real Time PCR (qRT-PCR) where a significant (P < 0.001) increase in the level of mRNA of ATP1B2 was observed in REMSD rat brains (Figure 1C) as compared with free moving control, large platform control, recovery control and Prazosin treated rats
Summary
Sleep is amongst the most conserved instinctive behaviors. It has been classified into rapid eye movement sleep (REMS) and non-REMS. Disturbance including restriction, fragmentation or loss of REMS is associated with several acute as well as chronic psycho-somatic-behavioral dysfunctions (Van Dongen et al, 2003), cognitive and memory dysfunctions (Walker and Stickgold, 2014), neurodegenerative diseases, hypertension, diabetes, mood disorder, altered neuronal growth, development and excitability (Mallick and Singh, 2011). All these patho-physio-behavioral modulations can take place due to changes in the levels of one or more biomolecules or its metabolites or sometimes due to synthesis of new molecule(s). Regardless of the advances in our knowledge on regulation and function of REMS (Mallick et al, 2011), there are serious lacunae in our understanding of the molecular mechanism underlying REMS-loss associated alteration of physiological conditions and symptoms, its sustained long-term effects (Mehta et al, 2015)
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