ArticleThe Journal of physiology2002
Biphasic modulation of synaptic transmission by hypertonicity at the embryonic Drosophila neuromuscular junction.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 10 citations in OpenAlex.
- C2B polylysine motif of synaptotagmin facilitates a Ca2+-independent stage of synaptic vesicle priming in vivo.Molecular biology of the cell · 2006Article
- Dystrophin is required for appropriate retrograde control of neurotransmitter release at the Drosophila neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
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3 authors at 1 institution in 1 country.
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Abstract
Puff-application of hypertonic saline (sucrose added to external saline) causes a transient increase in the frequency of spontaneous miniature synaptic currents (mSCs) at the neuromuscular junctions of Drosophila embryos. The frequency gradually returns to pre-application levels. External Ca(2+) is not needed for this response, but it may modify it. At 50 mM added sucrose, for example, enhanced spontaneous release was observed only in the presence of external Ca(2+), suggesting that Ca(2+) augments the response. In a high-K(+) solution, in which the basal mSC frequency was elevated, higher sucrose concentrations produced an increase in mSC frequency that was followed (during and after the hypertonic exposure) by depression, with the magnitude of both effects increasing with hypertonicity between 100 and 500 mM. Evoked release by nerve stimulation showed only depression in response to hypertonicity. We do not believe that the depression of spontaneous or evoked release can be explained by the depletion of releasable quanta, however, since the frequency of quantal release did not reach levels compatible with this explanation and the enhancement and depression could be obtained independent of one another. In a mutant lacking neuronal synaptobrevin, only the depression of mSC frequency was induced by hypertonicity. Conversely, only the enhancing effect was observed in wild-type embryos when the mSC frequency was elevated with forskolin in Ca(2+)-free saline. In cultured embryonic Drosophila neurons, Ca(2+) signals that were induced by high K(+) and detected by Fura-2, were reduced by hypertonicity, suggesting that the depressing response is due to a direct effect of hypertonicity on Ca(2+) influx.
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