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 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.
Chao
K F
KF
Department of Pharmacology, National Taiwan University, Taipei.
Liu
S H
SH
Lin-Shiau
S Y
SY
D019297:2,4-Dinitrophenol / Q000494:pharmacology; D015761:4-Aminopyridine / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001386:Azides / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D051379:Mice; D008813:Mice, Inbred ICR; D009045:Motor Endplate / Q000187:drug effects*; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000494:pharmacology*; D019810:Sodium Azide; D012966:Sodium Cyanide / Q000494:pharmacology*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
D001386:Azides; D004791:Enzyme Inhibitors; D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D010042:Ouabain; D019789:Tetraethylammonium; D000255:Adenosine Triphosphate; D019810:Sodium Azide; D015761:4-Aminopyridine; D012966:Sodium Cyanide; D019297:2,4-Dinitrophenol; D011188:Potassium