Bruce Herring received a Ph.D. in the laboratory of Aaron Fox at the University of Chicago, where he began studying the molecular mechanisms of synaptic transmission. With a growing appreciation for the role synapses play in learning, memory and cognition, Herring went on to join the laboratory of Roger A. Nicoll at the University of California, San Francisco. Here, he accumulated a broad knowledge base regarding the molecular regulation of glutamatergic synapse function. Faced with mounting evidence in favor of glutamatergic synapse dysregulation contributing to the development of autism spectrum disorder (ASD), Herring has turned his attention toward understanding how synaptic function is perturbed in ASD-related disorders and identifying the molecules responsible for synaptic dysfunction.
The primary goal of the Herring laboratory is to understand how disruption of synapse function ultimately gives rise to ASD. Herring’s laboratory uses a combination of electrophysiology, optogenetics, super-resolution microscopy, molecular biology and rodent behavior analysis in order to identify the consequences of ASD-related mutations at the cellular and molecular level and understand how these consequences give rise to ASD-related behaviors. This comprehensive approach will have a significant impact on identifying new key molecules involved in the development of ASD that will be invaluable in developing novel therapeutics to treat these disorders.