ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Rac GTPase plays an essential role in exocytosis by controlling the fusion competence of release sites.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 56 citations in OpenAlex.
- KV 10.1 opposes activity-dependent increase in Ca²⁺ influx into the presynaptic terminal of the parallel fibre-Purkinje cell synapse.The Journal of physiology · 2015Article
- Rho GTPases, phosphoinositides, and actin: a tripartite framework for efficient vesicular trafficking.Small GTPases · 2014Review
- Activation of sphingosine 1-phosphate receptor-1 by SEW2871 improves cognitive function in Alzheimer's disease model rats.EXCLI journal · 2013Article
- Adaptation of granule cell to Purkinje cell synapses to high-frequency transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- A novel form of presynaptic plasticity based on the fast reactivation of release sites switched off during low-frequency depression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- The Rho guanine nucleotide exchange factors Intersectin 1L and β-Pix control calcium-regulated exocytosis in neuroendocrine PC12 cells.Cellular and molecular neurobiology · 2010Review
- Bacterial toxins and the nervous system: neurotoxins and multipotential toxins interacting with neuronal cells.Toxins · 2010Review
- The role of actin remodeling in the trafficking of intracellular vesicles, transporters, and channels: focusing on aquaporin-2.Pflugers Archiv : European journal of physiology · 2008Review
- Fast changes in the functional status of release sites during short-term plasticity: involvement of a frequency-dependent bypass of Rac at Aplysia synapses.The Journal of physiology · 2007Article
- Involvement of sphingosine-1-phosphate in glutamate secretion in hippocampal neurons.Molecular and cellular biology · 2007Article
- Clostridium sordellii lethal toxin kills mice by inducing a major increase in lung vascular permeability.The American journal of pathology · 2007Article
- Rho is a presynaptic activator of neurotransmitter release at pre-existing synapses in C. elegans.Genes & development · 2006Article
- Actin cytoskeletal reorganizations and coreceptor-mediated activation of rac during human immunodeficiency virus-induced cell fusion.Journal of virology · 2004Article
- Degeneration and regeneration of murine skeletal neuromuscular junctions after intramuscular injection with a sublethal dose of Clostridium sordellii lethal toxin.Infection and immunity · 2004Article
- Facilitation of Ca(2+)-dependent exocytosis by Rac1-GTPase in bovine chromaffin cells.The Journal of physiology · 2003Article
- Pharmacological inactivation of the small GTPase Rac1 impairs long-term plasticity in the mouse hippocampus.NeuropharmacologyArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of small GTPases of the Rho family in synaptic functions has been addressed by analyzing the effects of lethal toxin (LT) from Clostridium sordellii strain IP82 (LT82) on neurotransmitter release at evoked identified synapses in the buccal ganglion of Aplysia. LT82 is a large monoglucosyltranferase that uses UDP-glucose as cofactor and glucosylates Rac (a small GTPase related to Rho), and Ras, Ral, and Rap (three GTPases of the Ras family). Intraneuronal application of LT (50 nm) rapidly inhibits evoked acetylcholine (ACh) release as monitored electrophysiologically. Injection of the catalytic domain of the toxin similarly blocked ACh release, but not when key amino acids needed for glucosylation were mutated. Intraneuronal application of competitive nucleotide sugars that differentially prevent glucosylation of Rac- and Ras-related GTPases, and the use of a toxin variant that affects a different spectrum of small GTPases, established that glucosylation of Rac is responsible for the reduction in ACh release. To determine the quantal release parameters affected by Rac glucosylation, we developed a nonstationary analysis of the fluctuations in postsynaptic response amplitudes that was performed before and after the toxin had acted or during toxin action. The results indicate that neither the quantal size nor the average probability for release were affected by lethal toxin action. ACh release blockage by LT82 was only caused by a reduction in the number of functional release sites. This reveals that after docking of synaptic vesicles, vesicular Rac stimulates a membrane effector (or effectors) essential for the fusion competence of the exocytotic sites.
Indexed as
Identifiers
12223550PMC6758122W1517140397What 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.