ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Ceramidase regulates synaptic vesicle exocytosis and trafficking.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 103 citations in OpenAlex.
- Methodological Pitfalls of Investigating Lipid Rafts in the Brain: What Are We Still Missing?Biomolecules · 2024Review
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- Lipids and Secretory Vesicle Exocytosis.Advances in neurobiology · 2023Article
- Sphingosine kinase 2 regulates insulin receptor trafficking in hepatocytes.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Extracellular vesicles, from the pathogenesis to the therapy of neurodegenerative diseases.Translational neurodegeneration · 2022Review
- Proline Metabolism in Neurological and Psychiatric Disorders.Molecules and cells · 2022Review
- Neuronal activity induces glucosylceramide that is secreted via exosomes for lysosomal degradation in glia.Science advances · 2022Article
- RNA-binding FMRP and Staufen sequentially regulate the Coracle scaffold to control synaptic glutamate receptor and bouton development.Development (Cambridge, England) · 2022Article
- Perinatal Dietary Polyunsaturated Fatty Acids in Brain Development, Role in Neurodevelopmental Disorders.Nutrients · 2021Review
- Changes in Membrane Ceramide Pools in Rat Soleus Muscle in Response to Short-Term Disuse.International journal of molecular sciences · 2019Article
- ELOVL4: Very long-chain fatty acids serve an eclectic role in mammalian health and function.Progress in retinal and eye research · 2019Review
- Novel Cellular Functions of Very Long Chain-Fatty Acids: Insight From ELOVL4 Mutations.Frontiers in cellular neuroscience · 2019Review
- Homozygous Expression of Mutant ELOVL4 Leads to Seizures and Death in a Novel Animal Model of Very Long-Chain Fatty Acid Deficiency.Molecular neurobiology · 2018Article
- Lipid metabolic perturbation is an early-onset phenotype in adultMolecular biology of the cell · 2017Article
- The 16p11.2 homologs fam57ba and doc2a generate certain brain and body phenotypes.Human molecular genetics · 2017Article
- Sphingosine Kinase 1 Cooperates with Autophagy to Maintain Endocytic Membrane Trafficking.Cell reports · 2016Article
- A New Fiji-Based Algorithm That Systematically Quantifies Nine Synaptic Parameters Provides Insights into Drosophila NMJ Morphometry.PLoS computational biology · 2016Article
- Ceramides And Stress Signalling Intersect With Autophagic Defects In Neurodegenerative Drosophila blue cheese (bchs) Mutants.Scientific reports · 2015Article
- Sphingolipid metabolism correlates with cerebrospinal fluid Beta amyloid levels in Alzheimer's disease.PloS one · 2015Article
- Ceramides in Alzheimer's Disease: Key Mediators of Neuronal Apoptosis Induced by Oxidative Stress and Aβ Accumulation.Oxidative medicine and cellular longevity · 2015Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
A screen for Drosophila synaptic dysfunction mutants identified slug-a-bed (slab). The slab gene encodes ceramidase, a central enzyme in sphingolipid metabolism and regulation. Sphingolipids are major constituents of lipid rafts, membrane domains with roles in vesicle trafficking, and signaling pathways. Null slab mutants arrest as fully developed embryos with severely reduced movement. The SLAB protein is widely expressed in different tissues but enriched in neurons at all stages of development. Targeted neuronal expression of slab rescues mutant lethality, demonstrating the essential neuronal function of the protein. C(5)-ceramide applied to living preparations is rapidly accumulated at neuromuscular junction (NMJ) synapses dependent on the SLAB expression level, indicating that synaptic sphingolipid trafficking and distribution is regulated by SLAB function. Evoked synaptic currents at slab mutant NMJs are reduced by 50-70%, whereas postsynaptic glutamate-gated currents are normal, demonstrating a specific presynaptic impairment. Hypertonic saline-evoked synaptic vesicle fusion is similarly impaired by 50-70%, demonstrating a loss of readily releasable vesicles. In addition, FM1-43 dye uptake is reduced in slab mutant presynaptic terminals, indicating a smaller cycling vesicle pool. Ultrastructural analyses of mutants reveal a normal vesicle distribution clustered and docked at active zones, but fewer vesicles in reserve regions, and a twofold to threefold increased incidence of vesicles linked together and tethered at the plasma membrane. These results indicate that SLAB ceramidase function controls presynaptic terminal sphingolipid composition to regulate vesicle fusion and trafficking, and thus the strength and reliability of synaptic transmission.
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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.