ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Selective effects of neuronal-synaptobrevin mutations on transmitter release evoked by sustained versus transient Ca2+ increases and by cAMP.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 74 citations in OpenAlex.
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- Alteration in information flow through a pair of feeding command neurons underlies a form of Pavlovian conditioning in the Drosophila brain.Current biology : CB · 2021Article
- SNARE Regulatory Proteins in Synaptic Vesicle Fusion and Recycling.Frontiers in molecular neuroscience · 2021Review
- Electrophysiological analysis of synaptic transmission in Drosophila.Wiley interdisciplinary reviews. Developmental biology · 2017Review
- BDNF-induced endocannabinoid release modulates neocortical glutamatergic neurotransmission.Synapse (New York, N.Y.) · 2017Article
- Transmission, Development, and Plasticity of Synapses.Genetics · 2015Review
- Molecular underpinnings of synaptic vesicle pool heterogeneity.Traffic (Copenhagen, Denmark) · 2015Review
- Vesicle-associated membrane protein 2 (VAMP2) but Not VAMP3 mediates cAMP-stimulated trafficking of the renal Na+-K+-2Cl- co-transporter NKCC2 in thick ascending limbs.The Journal of biological chemistry · 2014Article
- Spontaneous and evoked release are independently regulated at individual active zones.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
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- Acute genetic manipulation of neuronal activity for the functional dissection of neural circuits-a dream come true for the pioneers of behavioral genetics.Journal of neurogenetics · 2012Review
- A model for sealing plasmalemmal damage in neurons and other eukaryotic cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
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- Cav2-type calcium channels encoded by cac regulate AP-independent neurotransmitter release at cholinergic synapses in adult Drosophila brain.Journal of neurophysiology · 2009Article
- Increased Ca2+ influx through Na+/Ca2+ exchanger during long-term facilitation at crayfish neuromuscular junctions.The Journal of physiology · 2007Article
- v-SNAREs control exocytosis of vesicles from priming to fusion.The EMBO journal · 2005Article
- Proteolysis of SNARE proteins alters facilitation and depression in a specific way.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
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- Unconventional myosin Myo1c promotes membrane fusion in a regulated exocytic pathway.Molecular and cellular biology · 2004Article
- Biphasic modulation of synaptic transmission by hypertonicity at the embryonic Drosophila neuromuscular junction.The Journal of physiology · 2002Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptobrevin is a key constituent of the synaptic vesicle membrane. The neuronal-synaptobrevin (n-syb) gene in Drosophila is essential for nerve-evoked synaptic currents, but miniature excitatory synaptic currents (mESCs) remain even in the complete absence of this gene. To further characterize the defect in these mutants, we have examined conditions that stimulate secretion. Despite the inability of an action potential to trigger fusion, high K+ saline could increase the frequency of mESCs 4- to 17-fold in a Ca2+-dependent manner, and the rate of fusion approached 25% of that seen in wild-type synapses under the same conditions. Similarly, the mESC frequency in n-syb null mutants could be increased by a Ca2+ ionophore, A23187, and by black widow spider venom. Thus, the ability of the vesicles to fuse in response to sustained increases in cytosolic Ca2+ persisted in the absence of this protein. Tetanic stimulation could also increase the frequency of mESCs, particularly toward the end of a train and after the train of stimuli. In contrast, these mutants did not respond to an elevation of cAMP induced by an activator of adenylyl cyclase, forskolin, or a membrane-permeable analog of cAMP, dibutyryl cAMP, which in wild-type synapses causes a marked increase in the mESC frequency even in the absence of external Ca2+. These results are discussed in the context of models that invoke a special role for n-syb in coupling fusion to the transient, local changes in Ca2+ and an as yet unidentified target of cAMP.
Indexed as
Identifiers
10087058PMC6786081W1593682547What OpenQuestion holds
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.