Behavioral Effects of Prenatal Sleep Deprivation

In the perinatal time, sleep is fundamental to promote the healthy growth of a newborn contributing to survival, brain development, mother-infant interactions, and the establishment of physiological and cognitive functions. Sleep deprivation (SD) is an increasingly prevalent problem in modern society, especially in pregnant women. Gestational SD was proved to pose the mothers at higher risk for mental illnesses and depression and to hinder survival and health outcomes in the newborn. However, effects on the offspring behavior were poorly explored. Here, I conducted a screening of early and adult life behaviors in hybrid C57Bl/6J-CAST/EiJ mice born from mothers experiencing SD in the embryonic days (E) 11-13, during E15-17, or from control dams (CTRL). These specific time windows are known to have a heightened sensitivity to environmental stimuli. Effects occurring in these periods hold the potential to impact the offspring’s health and well-being both in early- and late-life. The expression of multiple genes implicated in homeostatic mechanisms in response to sleep loss or other behavioral manipulations was found to be parent-of-origin dependent. Consequently, in this thesis, behavioral effects of prenatal SD were explored in both types of C57Bl/6J-CAST/EiJ hybrids. In infancy, prenatal SD impacted the weight at postnatal day (P) 7 and P18 and altered the USVs repertoire exhibited in response to maternal separation. Also, in the attachment test, females E15-17 increased their preference towards the mother. In adult males, an enhanced anxiety-like phenotype was detected in F1 E15-17 together with heightened sociability. In females, the E11-13 F1 group showed signs of hyperactive-like behavior both in infancy and adulthood, whereas F1R E15-17 offspring exhibited a risk-aversive phenotype. Overall, these findings provided evidence that prenatal SD influences behavioral traits in first-generation offspring both in early and adult life with gender-specific and parent-of-origin effects. This study will contribute to future investigations to identify individuals at risk for adverse effects of prenatal SD and to develop therapies aimed at mitigating or preventing these effects.