Ruthenium Red, a Novel Enhancer of K + Currents at Mouse Motor Nerve Terminals

• Published in: Neuropharmacology 1996-05, Vol.35 (5), p.615-623
• Main Authors: LIN, MIN-JON, LIN-SHIAU, SHOEI-YN
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; calcium current; Fundamental and applied biological sciences. Psychology; Membrane Potentials - drug effects; Mice; Mice, Inbred ICR; motor nerve terminal; Motor Neurons - drug effects; Muscle Contraction - drug effects; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ; Phrenic Nerve - drug effects; Potassium Channels - drug effects; potassium current; Ruthenium red; Ruthenium Red - pharmacology; transmitter release; Vertebrates: nervous system and sense organs
• ISSN: 0028-3908; 1873-7064
• DOI: 10.1016/0028-3908(96)84632-6

The effects of ruthenium red (RR) on transmitter release and pre-synaptic currents were studied in the mouse neuromuscular junction. The action of RR (10 μM) was shown not only in the complete suppression of nerve-evoked muscle contractions associated with the depression of endplate potential amplitudes but also in the partial inhibition of the amplitude of miniature-endplate potentials. However, the other ruthenium compounds, ruthenium chloride and tris (2,2-bipyridyl) ruthenium chloride did not significantly affect the neuromuscular transmission. In pre-synaptic waveform studies, the fast K +-current [IK (f)] as well as the Ca 2+-activated K +-current [IK (ca)] was significantly enhanced by 10 μM RR. Furthermore, 10 μM RR antagonized the action of β-bungarotoxin (a blocker of slow K +-channel [IK (s)] in enhancing pre-synaptic Ca 2+ currents. In contrast, the typical Ca 2+-channel blockers, ω-agatoxin (0.5 μM), Gd 3 + (0.5 mM) and Cd 2 + (0.3 mM) all suppressed the IK (ca). Although RR (1–30 μM) inhibited the Ca 2+-currents of the nerve terminals induced by the combined treatment with the K +-channel blockers, 3,4-diaminopyridine plus tetraethylammonium chloride in a concentration-dependent manner, it is considered that RR-enhanced K + currents were responsible for, at least in part, the observed inhibition of the Ca 2+-current which led to the blockade of transmitter release. Copyright © 1996 Elsevier Science Ltd