The Mechanism of LTX^N4C-Induced Ca²⁺ Influx Involves Latrophilin-Mediated Activation of Ca_v2.x Channels.

ABSTRACT: Store-operated Ca²⁺ entry (SOCE) is a key regulator of cytosolic Ca²⁺ (Ca²⁺_cyt). Presynaptic SOCE can be activated by ligands like α-latrotoxin, which acts through the presynaptic G-protein-coupled receptor latrophilin-1 (LPHN1), inducing Ca²⁺ influx and neurotransmitter release. To understand how SOCE-associated proteins contribute to LPHN1 signaling in neurons, we used mouse neuroblastoma NB2a cells as a genetically tractable neuronal model. The cells were stably transfected with exogenous LPHN1 or its non-signaling mutant and stimulated with the non-pore-forming α-latrotoxin mutant LTX^N4C, a known trigger of neurotransmitter release. LPHN1 expression increased the proportion of neuron-like cells and upregulated the voltag

SUBMITTER: Blackburn JK 

PROVIDER: S-EPMC12653939 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature