| Popis: |
Autism spectrum disorder (ASD) is a developmental disorder characterized by impaired social interaction, language deficits, restricted interests, and stereotypic behavior. Autism is additionally associated with attention deficits, intellectual disabilities, and hyperactivity. Despite its recent increase in prevalence, the neural underpinnings of autism remain unclear. This research project investigates the neural substrates underlying attention deficits in a novel model of autism. Specifically, we measure non-selective attention (NSA) in 6-8 week old mice injected with a serotonin 1B agonist (RU24969) to induce autism-like behaviors. NSA is the spreading of attention across a visual field and is indexed by average rearing duration (ARD) in mice in an “open field chamber.” Mice are then injected with either atomoxetine, an approved treatment for ADHD, or a nitric oxide synthase inhibitor23 7-NINA, a drug found to treat NSA deficits in animal studies. We hypothesized that RU24969 would decrease ARD and, thus, NSA. Similarly, we expected RU24969 to increase overall locomotion in the open field. We also hypothesized that atomoxetine and 7-NINA would reverse NSA deficits induced by RU24969. Our results confirmed our hypothesis that RU24969 decreases ARD and increases locomotion. Our results also indicated that neither atomoxetine nor 7-NINA increased ARD alone or following RU24969 treatments. Unexpectedly, atomoxetine significantly exacerbated the NSA deficits induced by RU24969. Our findings replicate the findings of autism-like behavior following RU24969 challenge, and suggest that the putative treatments atomoxetine and 7-NINA will not be effective for treating the NSA deficits in ASD. |
