Early-life sleep disruption impairs subtle social behaviours in prairie voles: a pose-estimation study.

Early-life sleep disruption (ELSD) has been shown to have long-lasting effects on social behaviour in adult prairie voles (), including impaired expression of pair bonding during partner preference testing. However, due to the limitations of manual behaviour tracking, the effects of ELSD across the time course of pair bonding have not yet been described, hindering our ability to trace mechanisms. Here, we used pose estimation to track prairie voles during opposite-sex cohabitation, the process leading to pair bonding.

Early life sleep disruption has long lasting, sex specific effects on later development of sleep in prairie voles.

In mammals, sleep duration is highest in the early postnatal period of life and is critical for shaping neural circuits that control the development of complex behaviors. The prairie vole is a wild, highly social rodent that serves as a unique model for the study of complex, species-typical social behaviors. Previous work in our laboratory has found that early life sleep disruption (ELSD) in prairie voles during a sensitive window of postnatal development leads to long lasting changes in social and cognitive behaviors as well as structural changes in excitatory and inhibitory neural circuits in the brain.

Loss of sleep when it is needed most - Consequences of persistent developmental sleep disruption: A scoping review of rodent models.

Sleep is an essential component of development. Developmental sleep disruption (DSD) impacts brain maturation and has been associated with significant consequences on socio-emotional development. In humans, poor sleep during infancy and adolescence affects neurodevelopmental outcomes and may be a risk factor for the development of autism spectrum disorder (ASD) or other neuropsychiatric illness.

MEF2 is a key regulator of cognitive potential and confers resilience to neurodegeneration.

Recent increases in human longevity have been accompanied by a rise in the incidence of dementia, highlighting the need to preserve cognitive function in an aging population. A small percentage of individuals with pathological hallmarks of neurodegenerative disease are able to maintain normal cognition. Although the molecular mechanisms that govern this neuroprotection remain unknown, individuals that exhibit cognitive resilience (CgR) represent a unique source of therapeutic insight.