Grant: CIHR Fellowship

Autism spectrum disorder (ASD) is characterized by impairments in social communication and restricted interests. Several genes have been implicated in ASD, but a group of genes in the neuronal nBAF complex have emerged as promising candidates. The nBAF complex changes the structure of DNA to influence the way several genes are expressed in a cell. To date, no research has been conducted on the role of nBAF within neuron subtypes. I will investigate the loss of the nBAF complex specifically in inhibitory neurons in mice. Parvalbumin neurons are the most abundant type of inhibitory neuron in the brain and are frequently impaired in ASD. I hypothesize that loss of the nBAF complex will alter gene expression that is necessary for proper neuron function and resulting in ASD-like behaviours. Mice lacking the nBAF complex will undergo behavioural tests that can be used as a proxy to study ASD. The electrophysiological properties of neurons in mice lacking the nBAF complex will be measured to assess neuron function. Next generation sequencing will be employed to investigate alterations in gene expression. This work will be the first to test how loss of the nBAF complex specifically in PV neurons might lead to behavioural changes relevant to ASDs, providing the foundation for potential treatments.