α-Latrotoxin

α-Latrotoxin stimulates insulin C-peptide release to approximately 10 times basal secretion in HIT-T15 cells expressing full-length LPH^[5].

α-Latrotoxin triggers Ca²⁺-dependent norepinephrine release in synaptosomes; neurexin 1α and CL1 are required for distinct components of α-Latrotoxin-evoked glutamate release^[1].
α-Latrotoxin stimulates glutamate release in cultured cortical astrocytes^[1].

α-Latrotoxin spontaneously inserts into black lipid membranes to form stable cation channels with the highest conductance for Ca²⁺ and Mg²⁺, which are inhibited by Cd²⁺ and Ni²⁺; it also forms high-molecular-weight complexes, existing as dimers in the absence of divalent cations and as tetramers in their presence^[1].
α-Latrotoxin binds recombinant neurexins and CL1/CL2, and neurexin binding requires micromolar Ca^2+[1].
α-Latrotoxin triggers exocytosis in naive PC12 cells, whereas transfection of neurexin or CL1 increases sensitivity by 10- to 100-fold through a mechanism that does not require the receptor cytoplasmic domain^[1].
α-Latrotoxin produces dose-dependent massive acetylcholine release at frog neuromuscular junctions, ranging from subnanomolar levels that increase miniature currents to nonspecific membrane disintegration at >10 nM^[1].
α-Latrotoxin opens Ca²⁺ channels in Xenopus oocytes only after expression of brain mRNA, indicating that receptor binding is required for channel formation^[1].
α-Latrotoxin induces rapid contracture and loss of twitch tension in isolated chick biventer cervicis nerve-muscle preparations; evokes neuropeptide-mediated responses in guinea pig primary afferent and enteric nerve preparations; induces CGRP receptor antagonist-sensitive smooth muscle responses in isolated vascular preparations; and triggers massive synaptic vesicle exocytosis in cultured adult mouse DRG neurons^[2].
α-Latrotoxin binds with high affinity to CIRL-transfected COS-7 cell membranes and rat brain membranes in a calcium-independent manner (recombinant receptor K_d 0.16 nM; brain membranes 0.28 nM)^[4].
α-Latrotoxin (1 nM) induces an approximately 2.5-fold increase in inositol phosphate accumulation in COS-7 cells transfected with CIRL, and this process is calcium-dependent^[4].
α-Latrotoxin (20-200 pM; 4-5 min) stimulates hGH secretion in CIRL-expressing bovine chromaffin cells at as low as 20 pM, whereas control cells require 200 pM, reflecting an approximately 10-fold increase in sensitivity conferred by CIRL overexpression^[4].
α-Latrotoxin (α-LTX) (50 nM; 15 min) binds to full-length LPH and truncated LPH-TD1/LPH-TD1-7 expressed in HIT-T15 cells with a K_d of approximately 0.25 nM^[5].
α-Latrotoxin (0.1-1 nM; 20 s) induces a strong amperometric secretory spike in PC12 cells^[5].
α-Latrotoxin (2 nM) induces phase I oscillatory and phase II sustained intracellular calcium elevation in HIT-T15 cells expressing full-length LPH and in native MIN6 cells, mediates cell depolarization, and inhibits repolarizing potassium currents; whereas HIT-T15 cells expressing the truncated LPH-TD1 only exhibit phase II calcium responses, undergo only slight depolarization, and do not generate phase I action potentials^[5].
α-Latrotoxin can cause rapid contracture and loss of twitch tension in the nerve-muscle preparation of the chick biventer cervicis muscle^[6].