Mammalian brain development requires the transmission of electrical signals between neurons, in particular via the NMDA (N-methyl-D-aspartate) class of glutamate receptors.  Loss of electrical activity during development increases neuronal cell death, prevents the formation of precise neural circuits, diminishes respiration and feeding, and may play an important role in congenital brain disorders such as fetal alcohol syndrome.  Despite the importance of prenatal electrical activity for normal brain development, little is known about the underlying mechanisms.  The long-term goal of my research program is to understand cellular and molecular events that link NMDA receptor function and other forms of electrical activity to the development of mature neurons with normal patterns of synaptic connectivity.  We use a combination of approaches including transgenic mice, molecular biology, biochemistry, pharmacology, anatomy, and cell culture.  The present focus of the lab is on electrical activity-regulated genes in developing sensory systems, as well as the relationship between NMDA receptor function, synaptic development, and cell death.