期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 105, 期 17, 页码 6427-6432出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0708814105
关键词
adenosine; neuromuscular junction; neurotransmitter release; synaptic vesicles
资金
- NIAAA NIH HHS [AA016513, R21 AA016513] Funding Source: Medline
- NINDS NIH HHS [NS 12782, R01 NS012782] Funding Source: Medline
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, 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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