TARGETED CHEMOGENETIC MODELS OF EARLY-ADOLESCENT SLEEP DISTURBANCE – METABOLIC CONSEQUENCES IN MICE

Increasing rates of obesity and poor sleep pose serious public-health concerns. This is especially concerning given that adolescents are getting less and less sleep as technology invades their bedrooms. Several studies identify early adolescence as a critical window for sleep and adipose tissue development – including its innervation. This suggests that poor sleep during this period might alter the normal development of adipose tissue and cause metabolic imbalance. To investigate whether adolescent sleep quality contributes to the emergence of metabolic dysfunctions later in life, we propose to establish new rodent models of reversible sleep deprivation to disturb sleep at specific developmental windows. Here we present preliminary data of our new chemogenetic model in young mice (postnatal days 21-54). Our approach targets the ventral tegmental area, an arousal-promoting nucleus, by stimulating GABAergic neurons in the ventral pallidum. To assess the sleep amounts and quality of these animals we record their neural (EcoG) and muscular (EMG) activity. We assessed metabolic parameters during and after sleep disturbances with metabolic cages (energy expenditure, respiratory exchange rate, food intake, weight, activity), adipose tissue histology and plasma collection (hormones and proteins). Our preliminary results indicate successful sleep deprivation concomitant with decreased respiratory exchange rate indicating a shift toward lipid oxidation as a primary energy source.