Thus, channels with lowered glycosylation levels will be less active at a given membrane potential, and the cell likely will be hypo-excitable. Interestingly, different sodium channel isoforms are expressed at different times and in different cell types, each with a unique glycosylation pattern. This question will be addressed through biochemical, molecular biological, and electrophysiological methods designed to correlate N-glycosylation patterns among sodium channel isoforms to changes in channel function. We are now trying to limit the cytoplasmic regions responsible for this isoform specific function using significant molecular biological as well as electrophysiological methods. In addition to these two major areas of interest, there are several other interests and collaborations that are being pursued actively.
Many neurotransmitter transporters are the sites of action of drugs of abuse and of therapy.
Thus, we will study how these proteins work, and determine how drugs such as cocaine, amphetamine, and Prozac alter transport activity. S.S. Tinkle, A.G. Koszowski, and S.R. Levinson. J. Gen. Physiol. PubMed File E. Bennett, and G.A. Kimmich. Evidence for several potential dependent steps along the transport cycle.