ArticleBritish journal of pharmacology2005
Modulation of Ca(2+)-dependent and Ca(2+)-independent miniature endplate potentials by phorbol ester and adenosine in frog.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 15 citations in OpenAlex.
- Adenosine Receptors in Developing and Adult Mouse Neuromuscular Junctions and Functional Links With Other Metabotropic Receptor Pathways.Frontiers in pharmacology · 2018Article
- Adenosine A2B and A3 receptor location at the mouse neuromuscular junction.Journal of anatomy · 2014Article
- GPCR mediated regulation of synaptic transmission.Progress in neurobiology · 2012Review
- LY 294002 inhibits adenosine receptor activation by a mechanism independent of effects on PI-3 kinase or casein kinase II.Purinergic signalling · 2005Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Phorbol esters and adenosine modulate transmitter release from frog motor nerves through actions at separate sites downstream of calcium entry. However, it is not known whether these agents have calcium-independent sites of action. We therefore characterised calcium independent miniature endplate potentials (mepps) generated in response to 4-aminoquinaldine (4-AQ(A)) and then compared the modulation of these mepps by phorbol esters and adenosine with that of normal calcium dependent mepps. Application of 30 microM 4-AQ(A) resulted in the appearance of a population of mepps with amplitudes greater than twice the total population mode (mepp(>2M)). In the presence of 4-AQ(A), K(+) depolarisation or hypertonicity increased the numbers of normal amplitude mepps (mepp(N)) but had no effect on the frequency of mepp(>2M) events, suggesting that mepp(>2M) are not dependent on calcium. Treatment with the botulinum toxin (Botx) fractions C, D, or E (which selectively cleave syntaxin, synaptobrevin and SNAP-25, respectively) produced equivalent reductions in both normal and 4-AQ(A) induced mepps, suggesting that both mepp populations have equal dependence on the intact SNARE proteins. Phorbol dibutyrate (PDBu, 100 nM) increased the frequencies of both populations of mepps recorded in the presence of 4-AQ(A). Adenosine (25 microM) selectively reduced the numbers of mepp(N) with no effect on the frequency of mepp(>2M) events. These results suggest that mepp(>2M) events released in response to 4-AQ(A) are dependent on intact forms of syntaxin, synaptobrevin and SNAP-25, but unlike mepp(N) are independent of a functional calcium sensor. The selective action of adenosine, to reduce the numbers of normal amplitude mepps without effecting the frequency of mepp(>2M) events, suggests that adenosine normally inhibits transmitter release through a mechanism that is dependent on the presence of a functional calcium sensor.
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