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• W2009551404 abstract "Excessive daytime sleepiness and associated alterations in REM sleep patterns are among the most characteristic non-muscular features of myotonic dystrophy (DM). The symptoms of DM are caused by an expanded C (C) UG repeat that sequesters muscleblind-like protein 1 (MBNL1) and MBNL2, proteins that regulates alternative splicing required for fetal to adult developments. A recent study strongly suggests that major pathological changes in the DM brain are attributable to MBNL2 sequestration by toxic RNAs and dysregulation of specific alternative splicing events required for normal adult CNS function. We thus performed sleep EEG/EMG evaluations on Mbnl1 and Mbnl2 knockout (KO) mice. Adult wild and KO mice of Mbnl1 or Mbnl2 at 6 month of age (Mbnl1; n = 7, Mbnl2; n = 8) were implanted with EEG and EMG electrodes along with E-mitters. Sleep deprivation was performed for 6 h after one full day of baseline by gentle handling. Mbnl1 and Mbnl2 KOs had normal amounts, and natural diurnal distributions, of wakefulness and NREM sleep in the 12:12 LD condition. Shorter sleep latency and modest wake fragmentation during dark periods (frequent/shorter wake episodes) were observed in the Mbnl2 KO mice. However, the most profound sleep phenotypes observed in the Mbnl2 KO mice were an increase in REM sleep amounts, associated with increased numbers of REM sleep episodes, and increased EEG theta power. This change was most notable during the dark/active period. No direct transition from Wake to REM sleep, an EEG/EMG phenotype equivalent to behavioral cataplexy, was seen in either WT or Mbnl2 KO mice. A change in REM sleep in Mbnl2 KOs was also observed during rebound sleep after a 6-h sleep deprivation period initiated at ZT 0, where a more profound REM sleep rebound was observed in Mbnl2 KO mice, compared to WT mice. These REM specific changes were not observed in the Mbnl1 KO mice. Our results indicate that Mbnl2, but not Mbnl1, KO mice exhibit increased REM sleep propensity, suggesting REM-associated sleep abnormality in Mbnl2 KO are caused by dysregulation of specific alternative splicing events in the brain, and this may be one of the most important sleep abnormalities in DM. REM sleep characteristics in DM might be a residual of infant-type REM sleep, as infants of altricial species, including human and mice, spend large majority of time in REM sleep." @default.
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• W2009551404 date "2013-12-01" @default.
• W2009551404 modified "2023-10-16" @default.
• W2009551404 title "Sleep phenotype characterization of peripheral and central mouse models of myotonic dystrophy" @default.
• W2009551404 doi "https://doi.org/10.1016/j.sleep.2013.11.528" @default.
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