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. 2021 Apr 29;10:e68274. doi: 10.7554/eLife.68274

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© 2021, Bhandari et al

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

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Figure 8. — Schematic representation of the distribution and function of Cav2.3, GBRs, and KCTDs in ventral MHb terminals of WT and KCTD12b KO mice. Left: In WT terminals, the active zone contains Cav2.3 and hetero-pentameric rings comprising KCTD12b in excess over KCTD8, whereas KCTD8 and GBRs are located peri-synaptically. Right: In absence of KCTD12b, KCTD8 invades the active zone and compensates for the loss of KCTD12b, resulting in increased release probability, potentially via increased Ca²⁺ influx. See Figure 8—figure supplement 1.

Figure 8—figure supplement 1. — Schematic representation of the distribution and function of Cav2.3, GBRs, and KCTDs in ventral MHb terminals of WT and KCTD12b KO mice. Left: In WT terminals, the active zone contains Cav2.3 and hetero-pentameric rings comprising KCTD12b in excess over KCTD8, whereas KCTD8 and GBRs are located peri-synaptically. Right: In absence of KCTD12b, KCTD8 invades the active zone and compensates for the loss of KCTD12b, resulting in increased release probability, potentially via increased Ca²⁺ influx. See Figure 8—figure supplement 1.