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α-Latrotoxin Actions in the Absence of Extracellular Ca²⁺ Require Release of Stored Ca².

ABSTRACT: α-Latrotoxin (αLTX) causes exhaustive release of neurotransmitters from nerve terminals in the absence of extracellular Ca²⁺ (Ca²⁺_e). To investigate the mechanisms underlying this effect, we loaded mouse neuromuscular junctions with BAPTA-AM. This membrane-permeable Ca²⁺-chelator demonstrates that Ca²⁺_e-independent effects of αLTX require an increase in cytosolic Ca²⁺ (Ca²⁺_cyt). We also show that thapsigargin, which depletes Ca²⁺ stores, induces neurotransmitter release, but inhibits the effect of αLTX. We then studied αLTX's effects on Ca²⁺_cyt using neuroblastoma cells expressing signaling-capable or signaling-incapable variants of latrophilin-1, a G protein-

SUBMITTER: Blackburn JK

PROVIDER: S-EPMC11860464 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature

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α-Latrotoxin Actions in the Absence of Extracellular Ca²⁺ Require Release of Stored Ca².

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α-Latrotoxin Actions in the Absence of Extracellular Ca2+ Require Release of Stored Ca2.

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α-Latrotoxin Actions in the Absence of Extracellular Ca²⁺ Require Release of Stored Ca².