Changes of quantal transmitter release caused by gadolinium ions at the frog neuromuscular junction
Open Access
- 1 September 1991
- journal article
- Published by Wiley in British Journal of Pharmacology
- Vol. 104 (1) , 133-138
- https://doi.org/10.1111/j.1476-5381.1991.tb12397.x
Abstract
The actions of the trivalent cation, gadolinium (Gd3+), were studied on frog isolated neuromuscular preparations by conventional electrophysiological techniques. Gd3+(450 μm) applied to normal or formamide‐treated cutaneous pectoris nerve‐muscle preparations induced, after a short delay, a complete block of neuromuscular transmission. The reversibility of the effect was dependent on the time of exposure. Gd3+(5–450 μm) had no consistent effect on the resting membrane potential of the muscle fibres. Gd3+(5–40 μm) applied to preparations equilibrated in solutions containing high Mg2+and low Ca2+reduced the mean quantal content of endplate potentials (e.p.ps) in a dose‐dependent manner. Under those conditions, 3,4‐diaminopyridine (10 μm) consistently reversed the depression of evoked quantal release. The calcium current entering motor nerve terminals, revealed after blocking presynaptic potassium currents with tetraethylammonium (10 mm) in the presence of elevated extracellular Ca2+(8 mm), was markedly reduced by Gd3+(0.2–0.5 mm). Gd3+(40–200 μm) increased the frequency of spontaneous miniature endplate potentials (m.e.p.ps) in junctions bathed either in normal Ringer solution or in a nominally Ca2+‐free medium supplemented with 0.7 μm tetrodotoxin. This effect may be due to Gd3+entry into the nerve endings since it is not reversed upon removal of extracellular Gd3+with chelators (1 mm EGTA or EDTA). Gd3+also enhanced the frequency of me.p.ps appearing after each nerve stimulus in junctions bathed in a medium containing high Mg2+and low Ca2+ Gd3+, in concentrations higher than 100 μm, decreased reversibly the amplitude of m.e.p.ps suggesting a postsynaptic action. It is concluded that the block of nerve‐impulse evoked quantal release caused by Gd3+is related to its ability to block the calcium current entering the nerve endings, supporting the view that Gd3+blocks N‐type Ca2+channels; while the enhancement of spontaneous quantal release is probably the result of Gd3+entry into motor nerve endings. Besides its dual prejunctional effects on quantal release it is suggested that Gd3+exerts a postsynaptic action on the endplate acetylcholine receptor‐channel complex.Keywords
This publication has 28 references indexed in Scilit:
- Interactions Between α‐Latrotoxin and Trivalent Cations in Rat Striatal Synaptosomal PreparationsJournal of Neurochemistry, 1989
- Acetylcholine modulates two types of presynaptic potassium channels in vertebrate motor nerve terminalsNeuroscience Letters, 1986
- Blockade of transmitter release by a synthetic venom peptide, .OMEGA.-conotoxin.Proceedings of the Japan Academy, Series B, 1986
- A venom peptide with a novel presynaptic blocking actionNature, 1984
- The antagonism between botulinum toxin and calcium in motor nerve terminalsProceedings of the Royal Society of London. B. Biological Sciences, 1982
- A new method for excitation-contraction uncoupling in frog skeletal muscle.The Journal of cell biology, 1978
- Dual action of erbium on transmitter release at the frog neuromuscular synapseNature, 1978
- Responses of skeletal muscle fibres to lanthanide ions. Dependence of the twitch response on ionic radiiCellular and Molecular Life Sciences, 1977
- Effects of Rare Earths and Yttrium on Striated Muscle and the Neuromuscular JunctionCanadian Journal of Physiology and Pharmacology, 1972
- Effect of lanthanum ions on function and structure of frog neuromuscular junctionsProceedings of the Royal Society of London. B. Biological Sciences, 1971