Second, we examine mechanisms of hypoxic-ischemic injury of the brain's white matter. Relatively little is known about how white matter injury occurs in stroke, cerebral ischemia, and central nervous system trauma. We have found that overactivation of glutamate receptors is toxic not only to neurons, but also to oligodendrocytes, the myelin-forming glial cells. We are pursuing this surprising result to better understand pathways which lead to oligodendrocyte death. We are also using cell culture and brain slice models to understand mechanisms of axonal injury.
NMDA receptors mediate hypoxic spine loss in cultured neurons.
Distinct roles for sodium, chloride, and calcium in excitotoxic dendrite injury and recovery. Distinct roles for sodium, chloride, and calcium in excitotoxic dendritic injury and recovery. Calpain activation contributes to dendritic remodeling after brief excitotoxic injury in vitro. AMPA receptor activation is rapidly toxic to cortical astrocytes when desensitization is blocked.