ArticleBritish journal of pharmacology1994
Reduction by intracellular calcium chelation of acetylcholine secretion without occluding the effects of adenosine at frog motor nerve endings.
Article in British journal of pharmacology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 13 citations in OpenAlex.
- Modeling of the Glutamatergic Synaptic Transmission and its Modulation by Adenosine and Caffeine.Synapse (New York, N.Y.) · 2026Article
- Adenosine decreases both presynaptic calcium currents and neurotransmitter release at the mouse neuromuscular junction.The Journal of physiology · 2004Article
- Differential modulation of synaptic transmission by calcium chelators in young and aged hippocampal CA1 neurons: evidence for altered calcium homeostasis in aging.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Properties of spontaneous depolarizations in circular smooth muscle cells of rabbit urethra.British journal of pharmacology · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
1. The calcium chelators bis-(aminophenoxy)ethane-tetraacetic acid (BAPTA) or dimethyl-BAPTA (DMBAPTA) were introduced into the cytoplasm of frog motor nerve endings by use of the AM loading technique. The effects of intracellular Ca2+ chelation was studied on quantal acetylcholine (ACh) release and on the action of adenosine. 2. Intracellular BAPTA or DMBAPTA prevented the increases in quantal ACh secretion normally evoked by caffeine. 3. Intracellular DMBAPTA decreased the number of ACh quanta released by individual nerve impulses and virtually eliminated the fast phase of facilitation in response to paired nerve impulses. 4. Adenosine reduced both spontaneous and evoked secretion of ACh quanta with its usual potency and efficacy in the presence of intracellular DMBAPTA. Adenosine had no significant effect on facilitation. 5. The results, which suggest that adenosine and intracellular DMBAPTA reduce ACh secretion by different mechanisms, are consistent with the hypothesis that adenosine inhibits ACh release by reducing the ability of Ca2+ to promote ACh secretion from frog motor nerve endings.
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Registered trials
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