Skip to content Skip to navigation

Fundamental Themes in Neurosciences - Jeremy Dittman

May 28, 2015 - 12:00pm to 1:00pm
Clark Center Auditorium


Molecular control of synaptic vesicle fusion


Jeremy Dittman, MD, Ph.D. Associate Professor, Biochemistry Department, Weill Cornell Medical College

Host: Aaron Gitler


Synapses continually replenish their synaptic vesicle (SV) pools while suppressing spontaneous fusion events, thus maintaining a high dynamic range in response to physiological stimuli. The presynaptic protein complexin can both promote and inhibit fusion through interactions between its α-helical domain and the SNARE complex. We found that complexin's C-terminal half is required for two forms of inhibition.  First, a small curvature-sensing module within the C-terminal domain (CTD) directs complexin to SVs thereby positioning complexin to intercept the rapidly assembling SNAREs and control the rate of spontaneous fusion.  Second, neuromodulators acting through the inhibitory G-alpha subunit require the CTD of complexin to suppress neurotransmitter release.  In addition to neuromodulators, synaptic activity also affects complexin binding and localization within synaptic boutons, potentially contributing to use-dependent changes in synaptic transmission. Thus, the CTD plays a critical role in the control of synaptic transmission.

Event Sponsor: 
Stanford Neurosciences Institute
Contact Email:
Contact Phone: 

This event is part of: