This Trailblazer study investigates the role of purinergic signaling as a key component of, but previously unstudied mechanism of mitochondria-nuclear cross-talk, and as a regulator of synaptogenesis and neuroinflammation in a mouse model of autism spectrum disorders (ASD). If successful, this research will pioneer a completely new approach to therapy and open the door to a whole new class of drugs that can be developed and refined for the treatment of ASD. The investigators propose to document mitochondrial dysfunction and synapse pathology in the brains of mice in a mouse model of ASD. Dysfunction of genes involved in synaptogenesis has emerged as one of the most common unifying features in children with autism. This aim will build on the recent discovery that mitochondria in microglia profoundly influence normal synapse formation during development. The investigators will then test the effect of nucleotide receptor antagonists like Suramin in reducing synaptic pathology and treating ASD behaviors.