ArticlePflugers Archiv : European journal of physiology1989
Shifts in the voltage dependence of synaptic release due to changes in the extracellular calcium concentration at nerve terminals on muscle of crayfish and frogs.
Article in Pflugers Archiv : European journal of physiology, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Historical view and physiology demonstration at the NMJ of the crayfish opener muscle.Journal of visualized experiments : JoVE · 2009Article
- Contribution of Ca2+ inflow to quantal, phasic transmitter release from nerve terminals of frog muscle.Pflugers Archiv : European journal of physiology · 1992Article
- Evoked phasic release in frog nerve terminals obtained after block of Ca2+ entry by Cd2+.Pflugers Archiv : European journal of physiology · 1991Article
- Inhibition of Ca2+ inflow at nerve terminals of frog muscle blocks facilitation while phasic transmitter release is still considerable.Pflugers Archiv : European journal of physiology · 1990Article
- Calcium dependence of quantal release triggered by graded depolarization pulses to nerve terminals on crayfish and frog muscle.Pflugers Archiv : European journal of physiology · 1989Article
- Twin pulse facilitation in dependence on pulse duration and calcium concentration at motor nerve terminals of crayfish and frogs.Pflugers Archiv : European journal of physiology · 1989Article
- Calcium and depolarization dependence of twin-pulse facilitation of synaptic release at nerve terminals of crayfish and frog muscle.Pflugers Archiv : European journal of physiology · 1989Article
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1 author.
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Abstract
The rate of release of transmitter quanta, elicited by variable depolarization pulses applied to a nerve terminal by means of a macro-patch-clamp electrode, was measured in muscles of crayfish and frogs. The electrode was perfused with solutions containing different Ca concentrations, Cae. The bath was superfused separately, usually with solutions containing nominally no Cab and elevated Mgb. A fixed depolarization pulse followed the variable test pulse within 7-10 ms, and facilitation, Fc, of release after the fixed pulse was determined as a measure of Ca-inflow during the test pulse. As described before, Fc always showed a peak, Fc, at depolarization amplitudes of the test pulse below the saturation level of release. When Cae was changed, the depolarization levels generating Fc shifted in a negative direction if Cae was lowered, and in a positive direction if Cae was increased. These shifts agreed with the known dependence of the effective membrane potential (controlling e.g. Ca inward current) on Cae which is due to shielding of surface changes by Ca2+ (cf. Hille 1984). Changes of Cab, at constant Cae, did not affect the depolarization dependence of Fc. It is concluded that Ca inflow is not the only factor controlling quantal release, and that at least in depolarizations beyond those eliciting Fc another potential dependent factor increases release while Ca inflow presumably falls.
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