ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Synaptotagmin-2 is essential for survival and contributes to Ca2+ triggering of neurotransmitter release in central and neuromuscular synapses.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.
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136 citing papers in PubMed, 232 citations in OpenAlex.
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- Synaptotagmin isoforms differentially regulate glutamate and GABA release in the lateral habenula.bioRxiv : the preprint server for biology · 2026Article
- Disease-causing mutations in Synaptotagmin can act via dominant-negative, gain-of-function or haploinsufficient mechanisms.bioRxiv : the preprint server for biology · 2026Article
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- Immaturity of the neuromuscular junction in spinal muscular atrophy mouse models.Frontiers in cellular neuroscience · 2026Review
- Bltp1 Is Required for Survival and Normal Development and Function of the Neuromuscular Junction in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Harnessing synaptic vesicle release and recycling with antibody shuttle for targeted delivery of therapeutics to neurons.Molecular therapy. Methods & clinical development · 2025Article
- Distribution of mRNA for the exocytotic calcium sensor, synaptotagmin 9, in mouse brain.IBRO neuroscience reports · 2025Article
- Deciphering Auditory Hyperexcitability in Otogl Mutant Mice Unravels an Auditory Neuropathy Mechanism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Hippocampal gray matter volume alterations in patients with first-episode and recurrent major depressive disorder and their associations with gene profiles.BMC psychiatry · 2025Article
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- Parvalbumin interneurons: the dark and bright sides of a key playmaker of neural circuits and behavior.Frontiers in cellular neuroscience · 2025Review
- Cellular and synaptic specializations for sub-millisecond precision in the mammalian auditory brainstem.Frontiers in cellular neuroscience · 2025Review
- Toward discovering a novel family of peptides targeting neuroinflammatory states of brain microglia and astrocytes.Journal of neurochemistry · 2024Article
- Synaptotagmin-9 in mouse retina.Visual neuroscience · 2024Article
- Fast-spiking interneuron detonation drives high-fidelity inhibition in the olfactory bulb.PLoS biology · 2024Article
- Fast-spiking interneuron detonation drives high-fidelity inhibition in the olfactory bulb.bioRxiv : the preprint server for biology · 2024Article
- SYNAPTOTAGMIN-9 IN MOUSE RETINA.bioRxiv : the preprint server for biology · 2024Article
76 more citing papers are in PubMed but not listed here.
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9 authors at 2 institutions in 1 country.
Funding
Abstract
Biochemical and genetic data suggest that synaptotagmin-2 functions as a Ca2+ sensor for fast neurotransmitter release in caudal brain regions, but animals and/or synapses lacking synaptotagmin-2 have not been examined. We have now generated mice in which the 5' end of the synaptotagmin-2 gene was replaced by lacZ. Using beta-galactosidase as a marker, we show that, consistent with previous studies, synaptotagmin-2 is widely expressed in spinal cord, brainstem, and cerebellum, but is additionally present in selected forebrain neurons, including most striatal neurons and some hypothalamic, cortical, and hippocampal neurons. Synaptotagmin-2-deficient mice were indistinguishable from wild-type littermates at birth, but subsequently developed severe motor dysfunction, and perished at approximately 3 weeks of age. Electrophysiological studies in cultured striatal neurons revealed that the synaptotagmin-2 deletion slowed the kinetics of evoked neurotransmitter release without altering the total amount of release. In contrast, synaptotagmin-2-deficient neuromuscular junctions (NMJs) suffered from a large reduction in evoked release and changes in short-term synaptic plasticity. Furthermore, in mutant NMJs, the frequency of spontaneous miniature release events was increased both at rest and during stimulus trains. Viewed together, our results demonstrate that the synaptotagmin-2 deficiency causes a lethal impairment in synaptic transmission in selected synapses. This impairment, however, is less severe than that produced in forebrain neurons by deletion of synaptotagmin-1, presumably because at least in NMJs, synaptotagmin-1 is coexpressed with synaptotagmin-2, and both together mediate fast Ca2+-triggered release. Thus, synaptotagmin-2 is an essential synaptotagmin isoform that functions in concert with other synaptotagmins in the Ca2+ triggering of neurotransmitter release.
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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.