Epilepsy and autism are enigmatic neurodevelopmental disorders. Many different brain regions and cell types have been implicated, yet the mechanisms responsible for behavioral symptoms and physiological changes such as altered membrane excitability or synaptic transmission remain largely unknown.

The Anderson lab studies these disorders in mice, using molecular genetic techniques to design mouse models that bear human disease mutations or copy number variations. In some cases, the mutated genes are targeted for expression or deletion in specific brain regions or cell types, in order to map the seizure or behavioral disorder loci. These novel human disease models are then investigated using a diverse array of experimental approaches, including: patch-clamp electrophysiology to identify abnormalities in circuit function, biochemistry to identify defects in cell signaling, in vivo electrophysiology to measure the altered electrical activity occurring in epilepsy and behavior analysis to characterize features of autism spectrum disorder (such as impaired communication and social interaction and repetitive stereotypic behaviors).

The lab combines diverse technologies and experimental approaches to develop a program that combines a range of conditional genetic mouse models of disease, genome-wide transcriptional profiling, bioinformatics and protein interaction network analysis, cell-type targeted conditional viral vectors-based gene delivery, cell-type targeted conditional in vivo chemogenetics, and brain slice optogenetic patch clamp electrophysiology techniques with extensive behavioral analysis to understand the neuronal circuits and molecular mechanisms underlying genetic forms of human autism (e.g. maternal 15q11-13 triplications) and epilepsy. The Anderson team believes that these experimental approaches will set new standards for the study of molecular and circuit level dysfunction in mouse models of human neurobehavioral disorders.