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Suppression of potassium currents by cyanide on the mouse motor nerve terminals
NaCn at low concentrations markedly depressed the potassium currents in the motor nerve terminal of mouse triangularis sterni neuromuscular junction pretreated with potassium channel blockers 4-aminopyridine (4-AP), tetraethylammonium (TEA) or glucose-free medium. Neither azide nor dinitrophenol nor...
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Published in: | Neuroscience letters 1996-01, Vol.203 (2), p.105-108 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | NaCn at low concentrations markedly depressed the potassium currents in the motor nerve terminal of mouse triangularis sterni neuromuscular junction pretreated with potassium channel blockers 4-aminopyridine (4-AP), tetraethylammonium (TEA) or glucose-free medium. Neither azide nor dinitrophenol nor ouabain mimicked the effect of cyanide. This inhibitory effect of cyanide on nerve terminal spikes was correlated to its dramatic increase in spontaneous transmitter release under glucose-free condition. These results suggest that the effect of cyanide on the electrogenesis of nerve terminals is due to the direct suppression of ATP-sensitive K
+ current since the effect was antagonized by ATP-sensitive K
+ channels opener diazoxide and this may modulate the transmitter release. |
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ISSN: | 0304-3940 1872-7972 |
DOI: | 10.1016/0304-3940(95)12273-7 |