ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Presynaptic ryanodine receptors are required for normal quantal size at the Caenorhabditis elegans neuromuscular junction.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 91 citations in OpenAlex.
- Article
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- Article
- CaV1 and CaV2 calcium channels mediate the release of distinct pools of synaptic vesicles.eLife · 2023Article
- Regulation of Ryanodine Receptor-Dependent Neurotransmitter Release by AIP, Calstabins, and Presenilins.Advances in neurobiology · 2023Article
- Roles and Sources of Calcium in Synaptic Exocytosis.Advances in neurobiology · 2023Article
- Calcium Sensors of Neurotransmitter Release.Advances in neurobiology · 2023Article
- Synapsin Is Required for Dense Core Vesicle Capture and cAMP-Dependent Neuropeptide Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Presynaptic endoplasmic reticulum regulates short-term plasticity in hippocampal synapses.Communications biology · 2021Article
- Melatonin promotes sleep by activating the BK channel inProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Tissue-specific isoforms of the single C. elegans Ryanodine receptor gene unc-68 control specific functions.PLoS genetics · 2020Article
- Single Amino Acid Changes in the Ryanodine Receptor in the Human Population Have EffectsFrontiers in genetics · 2020Article
- Identification of avoidance genes through neural pathway-specific forward optogenetics.PLoS genetics · 2019Article
- Interactions among ryanodine receptor isotypes contribute to muscle fiber type development and function.Disease models & mechanisms · 2019Article
- Drosophila CaV2 channels harboring human migraine mutations cause synapse hyperexcitability that can be suppressed by inhibition of a Ca2+ store release pathway.PLoS genetics · 2018Article
- SNT-1 Functions as the CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Diverse modes of synaptic signaling, regulation, and plasticity distinguish two classes ofeLife · 2017Article
- AIP limits neurotransmitter release by inhibiting calcium bursts from the ryanodine receptor.Nature communications · 2017Article
- Retrograde Synaptic Inhibition Is Mediated by α-Neurexin Binding to the α2δ Subunits of N-Type Calcium Channels.Neuron · 2017Article
- Aging Effects ofG3 (Bethesda, Md.) · 2017Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Analyses of the effect of ryanodine in vertebrate brain slices have led to the conclusion that presynaptic ryanodine receptors (RYRs) may have several functions in synaptic release, including causing large-amplitude miniature postsynaptic currents (mPSCs) by promoting concerted multivesicular release. However, the role of RYRs in synaptic release is controversial. To better understand the role of RYRs in synaptic release, we analyzed the effect of RYR mutation on mPSCs and evoked postsynaptic currents (ePSCs) at the Caenorhabditis elegans neuromuscular junction (NMJ). Amplitudes of mPSCs varied greatly at the C. elegans NMJ. Loss-of-function mutations of the RYR gene unc-68 (uncoordinated 68) essentially abolished large-amplitude mPSCs. The amplitude of ePSCs was also greatly suppressed. These defects were completely rescued by expressing wild-type UNC-68 specifically in neurons but not in muscle cells, suggesting that RYRs acted presynaptically. A combination of removing extracellular Ca2+ and UNC-68 function eliminated mPSCs, suggesting that influx and RYR-mediated release are likely the exclusive sources of Ca2+ for synaptic release. Large-amplitude mPSCs did not appear to be caused by multivesicular release, as has been suggested to occur at vertebrate central synapses, because the rise time of mPSCs was constant regardless of the amplitude but distinctive from that of ePSCs, and because large-amplitude mPSCs persisted under conditions that inhibit synchronized synaptic release, including elimination of extracellular Ca2+, and mutations of syntaxin and SNAP25 (soluble N-ethylmaleimide-sensitive factor attachment protein 25). These observations suggest that RYRs are essential to normal quantal size and are potential regulators of quantal size.
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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.