| First Author | Dong W | Year | 2018 |
| Journal | Cell Rep | Volume | 24 |
| Issue | 2 | Pages | 284-293.e6 |
| PubMed ID | 29996090 | Mgi Jnum | J:269480 |
| Mgi Id | MGI:6259979 | Doi | 10.1016/j.celrep.2018.06.024 |
| Citation | Dong W, et al. (2018) CAST/ELKS Proteins Control Voltage-Gated Ca(2+) Channel Density and Synaptic Release Probability at a Mammalian Central Synapse. Cell Rep 24(2):284-293.e6 |
| abstractText | In the presynaptic terminal, the magnitude and location of Ca(2+) entry through voltage-gated Ca(2+) 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, Ca(2+) 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. |
