CAST/ELKS Proteins Control Voltage-Gated Ca2+ Channel Density and Synaptic Release Probability at a Mammalian Central Synapse

• DOI: 10.1016/j.celrep.2018.06.024
• Publication Date: 2018-07-11T18:09:28Z
• Authors: Wei Dong; Tamara Radulovic; R. Oliver Goral; Connon Thomas; Monica Suarez Mon...; Debbie Guerrero-G...; Akari Hagiwara; Travis Putzke; Yamato Hida; Manabu Abe; Kenji Sakimura; Naomi Kamasawa; Toshihisa Ohtsuka; Samuel M. Young
• Keywords: Neurotransmitter Agents; 0303 health sciences; QH301-705.5; Action Potentials; Nerve Tissue Proteins; Synaptic Transmission; Article; Mice, Inbred C57BL; Cytoskeletal Proteins; Kinetics; 03 medical and health sciences; Calcium Channels, N-Type; rab GTP-Binding Proteins; Synapses; Animals; Biology (General); Carrier Proteins; Ion Channel Gating; Probability

In the presynaptic terminal, magnitude and location of Ca2+ entry through voltage-gated channels (VGCCs) regulate efficacy neurotransmitter release. However, how active zone proteins control mammalian VGCC levels organization is unclear. To address this, we deleted CAST/ELKS protein family at calyx Held, a CaV2.1 channel-exclusive terminal. We found that loss reduces current density with concomitant reductions in channel numbers clusters. Surprisingly, deletion increases release probability while decreasing readily releasable pool, no change ultrastructure. addition, coupling unchanged, but spontaneous rates are elevated. Thus, our data identify distinct roles for as positive regulators suggest they post-priming step controls synaptic vesicle fusogenicity.