Duke Institute for Brain Sciences

Dr. Augustine's lab is interested in the function of synaptic connections between nerve cells. Experiments in the lab employ electrophysiological, molecular biological, and imaging methods to study the activity of single synapses. Attention is focused on two general questions. First, Dr. Augustine and his colleagues are examining the molecular basis of neurotransmitter release. They are exploring the molecular mechanisms that transduce a rise in neuronal Ca concentration into the exocytotic secretion of neurotransmitters, focusing on identifying the roles of proteins that are associated with synaptic vesicles. Second, they are examining the signal transduction pathways underlying long-lasting synaptic plasticity. Their work has identified the role of second messengers, such as Ca and IP3, in mediating long-term synaptic depression in the cerebellum. They are now examining how these signals are converted into the long-lasting changes in glutamate receptor function that yield long-term depression.

Postdoc, University of California, Los Angeles, 1980-1983

Ph.D., University of Maryland, College Park, 1980

B.S., University of Maryland, College Park, 1975

Gitler D, Cheng Q, Greengard P, Augustine GJ (2008). Synapsin IIa controls the reserve pool of glutamatergic synaptic vesicles. J Neurosci. 28(43):10835-43.

Zhao S, Cunha C, Zhang F, Liu Q, Gloss B, Deisseroth K, Augustine GJ, Feng G. (2008). Improved expression of halorhodopsin for light-induced silencing of neuronal activity. Brain Cell Biol. 36(1-4):141-54.

Tanaka K, Augustine GJ. (2008). A positive feedback signal transduction loop determines timing of cerebellar long-term depression. Neuron 59(4):608-20.