ArticleProceedings of the National Academy of Sciences of the United States of America2008
Selective disruption of the mammalian secretory apparatus enhances or eliminates calcium current modulation in nerve endings.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Purinergic Tuning of the Tripartite Neuromuscular Synapse.Molecular neurobiology · 2023Review
- Quantitative Proteomic Analysis Reveals Molecular Adaptations in the Hippocampal Synaptic Active Zone of Chronic Mild Stress-Unsusceptible Rats.The international journal of neuropsychopharmacology · 2015Article
- Modulation of neurotransmission by GPCRs is dependent upon the microarchitecture of the primed vesicle complex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Purinergic signalling in the musculoskeletal system.Purinergic signalling · 2013Review
- Evidence for constitutively-active adenosine receptors at mammalian motor nerve endings.European journal of pharmacology · 2012Article
- GPCR mediated regulation of synaptic transmission.Progress in neurobiology · 2012Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Modulation of secretion via G protein-coupled receptors (GPCRs) serves an important regulatory function in neuronal and nonneuronal secretory cells. Most secretory cells possess voltage-gated calcium channels, share homologues of the core complex of three proteins (the SNAREs) that constitute the secretory apparatus, and are modulated by GPCR activation. Activators of GPCRs generally inhibit the release of neurotransmitter substances to a maximum of only 50-60% of the control level, suggesting that complex protein-protein interactions may govern the efficacy of this form of modulation. In this article, molecular genetic approaches are used in combination with botulinum toxins (selective molecular scalpels that cleave the SNAREs at highly restricted loci) to address this issue. The results suggest that the cleavage of either of the plasma membrane SNAREs (syntaxin or SNAP-25) prevents modulation of calcium currents by A(1) adenosine receptors at mammalian motor nerve endings. In contrast, cleavage of the synaptic vesicle SNARE (synaptobrevin) in conjunction with deletion of the vesicle-docking protein Rab3A greatly enhances the efficacy of calcium current modulation.
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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.