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Abstract

Sleep deprivation studies indicate an essential role for sleep in the pathophysiology of many conditions, with sleep at a lifetime maximum during early life. Previous research in our lab using an early life sleep disruption (ELSD) paradigm has shown long lasting deficits in complex social and cognitive behaviors in adult prairie voles. We hypothesized that increased time spent awake during ELSD may cause a transient increase in excitatory neurotransmission, leading to morphological changes in dendritic spines and long lasting changes in excitatory neurotransmission

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