Autism spectrum disorders (ASDs) affect nearly 3% of the population, and the prevalence has increased more than 150% since 2000. Patients with autism suffer from impaired cognitive function, working memory, social interaction, and attention deficits. 

Fragile X syndrome (FXS) is the most known monogenic cause of autism. Behavioral and imaging studies revealed a shared neurobiological basis of autism between FXS and other ASDs. Although molecular and cellular data lag behind these studies, published data suggest common signaling pathways between FXS and other ASDs. 

The Brager Lab previously identified changes in voltage-gated ion channels in both the hippocampus and prefrontal cortex of the Fmr1 knockout (KO) mouse model of FXS. These channelopathies affect synaptic transmission, plasticity and the integration and transformation of synaptic inputs into output. Dr. Brager will present data showing that FMRP, the protein missing in FXS, bidirectionally regulates dendritic h-channels in a brain-region and cell-type specific manner. He will then present more recent data looking at how dendritic excitability in the prefrontal cortex is altered in FXS. The data suggest that these channelopathies and associated changes in dendritic integration alter hippocampal and prefrontal circuits and contribute to behavioral phenotypes associated with FXS.