Ben A. Barres

Professor of Neurobiology. Contributed to understanding the mechanisms that control formation of neural connections within the developing brain. Introduced methods to purify defined populations of neurons and glia to study the fundamental interactions that control synapse development, axon regeneration, and myelination. First to demonstrate CNS neurons have limited ability to form synapses unless signaled by glial cells. Lab identified the glial signal as thrombospondin and demonstrated that thrombospondin signals excitatory synaptogenesis through a neuronal receptor called ?-1. Dissecting the molecular domains responsible for this interaction, his lab elucidated the action of gabapentin, demonstrating that it antagonizes the binding of thrombospondin to 2 ?-1, a novel neuronal molecule required for synaptogenesis, and blocks new excitatory synapse formation in vitro and in vivo. Findings demonstrate the role of astrocytes in CNS synaptogenesis, with important implications for possible new pain medications. Identified the classical complement cascade as a key mediator of synapse elimination in the developing brain, suggesting that this cascade mediates the synapse loss driving neurodegenerative processes in Alzheimer's and other neurological diseases, which might then be treated with complement inhibitors.