UCLA

Nighttime light pollution is linked to metabolic and cognitive dysfunction. Many patients with autism spectrum disorders (ASD) show disturbances in their sleep/wake cycle and may be particularly vulnerable to the impact of circadian disruptors. We have previously shown that a 2-weeks exposure to dim light at night (DLaN, 5lx) disrupts diurnal rhythms and increases repetitive behaviors in the contactin-associated protein-like 2 knock-out (Cntnap2 KO) mouse model of autism. In addition, we found that short-wavelength enriched DLaN triggered cFos expression in the basolateral amygdala (BLA) raising the possibility that these cell populations may mediate the effects. Preliminary results revealed that DLaN increased the number of microglia, the brain resident immune cells that trigger inflammation. In this thesis, we examined the impact of exposure to DLaN on microglial density in the BLA and prefrontal cortex (PFC) of Cntnap2 mutant mice using Ionized Calcium Binding Adaptor Molecule 1 (Iba1) as a microglial molecular marker. 2-weeks daily treatment with DLaN evoked a mild increase in the number of Iba1+ cell in the BLA region. DLaN treatment of Cntnap2 KO mice increased microglia immunoreactivity in the PFC region. In addition, alterations in microglia evoked by DLaN were not specific to mutants as effects were also seen in WT mice. My data indicates that microglia may mediate the deleterious effects of circadian rhythm disruption by nighttime exposure to light in the Cntnap2 mouse model of autism. These findings suggest that circadian disruptors such as light at night should be considered in the management of ASD. Broadly, our findings are consistent with the recommendation that less exposure to light at night should be considered to optimize health in neurotypical as well as vulnerable populations.