AI Article Synopsis

  • Sleep disturbances are common in children with autism spectrum disorder (ASD) and are linked to the severity of their symptoms, especially memory issues.* -
  • In a study using a mouse model of ASD, researchers found that non-rapid eye movement sleep (NREMs) was fragmented, which correlated with increased activity in certain brain neurons during sleep.* -
  • By inhibiting these neurons, the study showed that sleep could be stabilized and memory improved, highlighting the significant role of the locus coeruleus noradrenergic system in regulating both sleep and memory in ASD.*

Article Abstract

Sleep disturbances are prevalent in children with autism spectrum disorder (ASD). Strikingly, sleep problems are positively correlated with the severity of ASD symptoms, such as memory impairment. However, the neural mechanisms underlying sleep disturbances and cognitive deficits in ASD are largely unexplored. Here, we show that non-rapid eye movement sleep (NREMs) is fragmented in the 16p11.2 deletion mouse model of ASD. The degree of sleep fragmentation is reflected in an increased number of calcium transients in the activity of locus coeruleus noradrenergic (LC-NE) neurons during NREMs. In contrast, optogenetic inhibition of LC-NE neurons and pharmacological blockade of noradrenergic transmission using clonidine consolidate sleep. Furthermore, inhibiting LC-NE neurons restores memory. Finally, rabies-mediated screening of presynaptic neurons reveals altered connectivity of LC-NE neurons with sleep- and memory-regulatory regions in 16p11.2 deletion mice. Our findings identify a crucial role of the LC-NE system in regulating sleep stability and memory in ASD.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11612818PMC
http://dx.doi.org/10.1016/j.isci.2024.111285DOI Listing

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