In central nervous system (CNS) synapses, action potential-evoked neurotransmitter release is principally mediated by CaV2.1 calcium channels (CaV2.1) and is highly dependent on the physical distance between CaV2.1 and synaptic vesicles (coupling). Although various active zone proteins are proposed to control coupling and abundance of CaV2.1 through direct interactions with the CaV2.1 α1 subunit C-terminus at the active zone, the role of these interaction partners is controversial. To define the intrinsic motifs that regulate coupling, we expressed mutant CaV2.1 α1 subunits on a CaV2.1 null background at the calyx of Held presynaptic terminal. Our results identified a region that directly controlled fast synaptic vesicle release and vesicle docking at the active zone independent of CaV2.1 abundance. In addition, proposed individual direct interactions with active zone proteins are insufficient for CaV2.1 abundance and coupling. Therefore, our work advances our molecular understanding of CaV2.1 regulation of neurotransmitter release in mammalian CNS synapses.
You may also like
The fruit fly and its comb-shaped neurons
February 1, 2021Ernst Strüngmann Institute for Neuroscience
Science on film, episode 4: Motivational states of the...
January 29, 2021Max Planck Institute for Biological Cybernetics
A small molecule involved in depression
January 29, 2021Max Planck Institute of Psychiatry
Max Planck Florida and Zeiss Announce Research...
January 13, 2021Max Planck Florida Institute for Neuroscience
New approach reveals structure and function of...
December 16, 2020Max Planck Florida Institute for Neuroscience
Targeting Functionally Characterized Synaptic...
December 15, 2020Max Planck Florida Institute for Neuroscience