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Journal Article

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

MPS-Authors

Dong,  Wei
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Radulovic,  Tamara
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Goral,  R. Oliver
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Thomas,  Connon
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Suarez Montesinos,  Monica
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Guerrero-Given,  Debbie
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Putzke,  Travis
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Kamasawa,  Naomi
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Young,  Samuel M.
Max Planck Florida Institute for Neuroscience, Max Planck Society;

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Citation

Dong, W., Radulovic, T., Goral, R. O., Thomas, C., Suarez Montesinos, M., Guerrero-Given, D., et al. (2018). CAST/ELKS Proteins Control Voltage-Gated Ca2+ Channel Density and Synaptic Release Probability at a Mammalian Central Synapse. Cell Reports, 284-293.e6. Retrieved from http://www.sciencedirect.com/science/article/pii/S2211124718309197.


Cite as: https://hdl.handle.net/21.11116/0000-0003-D51A-0
Abstract
Summary
In the presynaptic terminal, the magnitude and location of Ca2+ entry through voltage-gated Ca2+ channels (VGCCs) regulate the efficacy of neurotransmitter release. However, how presynaptic active zone proteins control mammalian VGCC levels and organization is unclear. To address this, we deleted the CAST/ELKS protein family at the calyx of Held, a CaV2.1 channel-exclusive presynaptic terminal. We found that loss of CAST/ELKS reduces the CaV2.1 current density with concomitant reductions in CaV2.1 channel numbers and clusters. Surprisingly, deletion of CAST/ELKS increases release probability while decreasing the readily releasable pool, with no change in active zone ultrastructure. In addition, Ca2+ channel coupling is unchanged, but spontaneous release rates are elevated. Thus, our data identify distinct roles for CAST/ELKS as positive regulators of CaV2.1 channel density and suggest that they regulate release probability through a post-priming step that controls synaptic vesicle fusogenicity.