ArticleProceedings of the National Academy of Sciences of the United States of America2005
Proteolysis of SNARE proteins alters facilitation and depression in a specific way.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Autaptic Cultures: Methods and Applications.Frontiers in synaptic neuroscience · 2020Article
- The role of synaptobrevin1/VAMP1 in Ca2+-triggered neurotransmitter release at the mouse neuromuscular junction.The Journal of physiology · 2011Article
- Gβγ and the C terminus of SNAP-25 are necessary for long-term depression of transmitter release.PloS one · 2011Article
- Opposing functions of two sub-domains of the SNARE-complex in neurotransmission.The EMBO journal · 2010Article
- Review
- Structural determinants of synaptobrevin 2 function in synaptic vesicle fusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Isoflurane depresses hippocampal CA1 glutamate nerve terminals without inhibiting fiber volleys.BMC neuroscience · 2006Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms of short-term plasticity observed during synaptic transmission are unknown. To determine whether the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins play a role in short-term plasticity, Botulinum toxins A, E, and F, were used to disrupt SNARE protein function in cultured hippocampal neurons. Although low concentrations of all of the toxins significantly reduced evoked release, they differentially affected short-term plasticity as assessed by the paired-pulse ratio, regardless of the initial release probability and size of the readily releasable pool of the synapse. The toxin effects on the paired-pulse ratio resulted in different phenotypes dependent on the toxin cleavage site. Together, these data indicate proteolysis of SNARE proteins alters facilitation and depression in a specific way.
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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.