ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
The alpha-latrotoxin mutant LTXN4C enhances spontaneous and evoked transmitter release in CA3 pyramidal neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 54 citations in OpenAlex.
- Latrophilin-1-Mediated GCells · 2026Article
- The Mechanism of LTXInternational journal of molecular sciences · 2025Article
- The Dissociation of Latrophilin Fragments by Perfluorooctanoic Acid (PFOA) Inhibits LTXToxins · 2025Article
- Article
- Structural basis of α-latrotoxin transition to a cation-selective pore.Nature communications · 2024Article
- Article
- ADGRL1 haploinsufficiency causes a variable spectrum of neurodevelopmental disorders in humans and alters synaptic activity and behavior in a mouse model.American journal of human genetics · 2022Article
- Molecular architecture of black widow spider neurotoxins.Nature communications · 2021Article
- Adhesion GPCRs as a paradigm for understanding polycystin-1 G protein regulation.Cellular signalling · 2020Review
- Discovery of a Recombinant Human Monoclonal Immunoglobulin G Antibody Against α-Latrotoxin From the Mediterranean Black Widow Spider (Frontiers in immunology · 2020Article
- Catching Latrophilin With Lasso: A Universal Mechanism for Axonal Attraction and Synapse Formation.Frontiers in neuroscience · 2019Review
- Article
- Expression of functional neuronal receptor latrophilin 1 in human acute myeloid leukaemia cells.Oncotarget · 2016Article
- International Union of Basic and Clinical Pharmacology. XCIV. Adhesion G protein-coupled receptors.Pharmacological reviews · 2015Review
- Different transporter systems regulate extracellular GABA from vesicular and non-vesicular sources.Frontiers in cellular neuroscience · 2013Article
- Adhesion G protein-coupled receptors: signaling, pharmacology, and mechanisms of activation.Molecular pharmacology · 2012Review
- Latrophilin 1 and its endogenous ligand Lasso/teneurin-2 form a high-affinity transsynaptic receptor pair with signaling capabilities.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Alpha-latrotoxin rescues SNAP-25 from BoNT/A-mediated proteolysis in embryonic stem cell-derived neurons.Toxins · 2011Article
- The latrophilins, "split-personality" receptors.Advances in experimental medicine and biology · 2010Review
- Penelope's web: using alpha-latrotoxin to untangle the mysteries of exocytosis.Journal of neurochemistry · 2009Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Alpha-latrotoxin (LTX) stimulates vesicular exocytosis by at least two mechanisms that include (1) receptor binding-stimulation and (2) membrane pore formation. Here, we use the toxin mutant LTX(N4C) to selectively study the receptor-mediated actions of LTX. LTX(N4C) binds to both LTX receptors (latrophilin and neurexin) and greatly enhances the frequency of spontaneous and miniature EPSCs recorded from CA3 pyramidal neurons in hippocampal slice cultures. The effect of LTX(N4C) is reversible and is not attenuated by La3+ that is known to block LTX pores. On the other hand, LTX(N4C) action, which requires extracellular Ca2+, is inhibited by thapsigargin, a drug depleting intracellular Ca2+ stores, by 2-aminoethoxydiphenyl borate, a blocker of inositol(1,4,5)-trisphosphate-induced Ca2+ release, and by U73122, a phospholipase C inhibitor. Furthermore, measurements using a fluorescent Ca2+ indicator directly demonstrate that LTX(N4C) increases presynaptic, but not dendritic, free Ca2+ concentration; this Ca2+ rise is blocked by thapsigargin, suggesting, together with electrophysiological data, that the receptor-mediated action of LTX(N4C) involves mobilization of Ca2+ from intracellular stores. Finally, in contrast to wild-type LTX, which inhibits evoked synaptic transmission probably attributable to pore formation, LTX(N4C) actually potentiates synaptic currents elicited by electrical stimulation of afferent fibers. We suggest that the mutant LTX(N4C), lacking the ionophore-like activity of wild-type LTX, activates a presynaptic receptor and stimulates Ca2+ release from intracellular stores, leading to the enhancement of synaptic vesicle exocytosis.
Indexed as
Identifiers
12764091PMC6741093W2149161655What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.