Sleep is a critical to health and wellbeing, and lack of sleep can have numerous detrimental
effects on human health. These effects can be overrepresented or exasperated in certain
populations, such as those with autism spectrum disorders (ASD). Mutations in the Shank3DC
gene have been used as a mouse model of autism, and these mice have been shown to have a
distinct sleep phenotype. A popular measure of sleep deprivation effects is Novel Object
Recognition (NOR), as sleep-deprived (SD) mice show disruptions to learning and memory.
Sleep is hypothesized to play a key role in memory consolidation through homeostatic synaptic
downscaling. Some key proteins involved in or mediating this process are Arc and mGluR5. The
current study will analyze behavioral and molecular changes following SD in juvenile mice by
administration of NOR to wild-type (WT) mice and Western Blotting of forebrains of WT and
Shank3WT/DC mice for protein quantification. Due to their vulnerability, I hypothesized lack of
novel object identification in NOR following both two-hour and four-hour sleep deprivation. I
also expected increase of Arc, mGluR5, and SHANK3, with Shank3WT/DC animals having more
intense responses. The study found juvenile WT mice to successfully learn only following a two-hour
sleep deprivation, indicating a limited tolerance. Arc showed significant increase post sleep
deprivation in both genotypes, while SHANK3 effects were only observed in Shank3WT/DC mice.
Contrary to the hypothesis, mGluR5 did not show variability among groups. Further study is
suggested with specified procedural modifications and larger data samples to include sex as a
variable of analysis
