Friday, October 28, 2011
Hall 1-2 (San Jose Convention Center)
Understanding the process of how the neurotransmitters are released by Ca 2+ -triggered exocytosis is an essential component to understanding the functionality of the nervous system. It has been found that during exocytosis a fusion pore is formed as intermediate between the vesicle docking on the cell membrane and releasing neurotransmitters; however, the mechanism of how the fusion pore is formed still remains a mystery. There are two hypotheses for the initial fusion pore, the lipid pore, and the protein pore. In a lipid pore, lipid bilayers become exceedingly curved. In this case, vesicle size plays a major role in fusion pore stability. Amperometry data supports the hypothesis that the initial pore is protein, and that membrane curvature occurs only after the protein pore starts to expand. Previous research conducted in the lab, indicated that the curvature of the membrane has a major impact on fusion pore stability. From this data, we hypothesized that that the initial fusion pore is formed with assistance from proteins, specifically SNARE proteins. N-bar domain, a membrane bending protein, has been found to induce positive curvature in membranes. Using Amperometry techniques, we analyzed the effects N-bar had on the fusion pore stability of PC12 cells. We propose that N-bar domain will affect the stability of the fusion pore.