دورية أكاديمية
Methocarbamol blocks muscular Nav1.4 channels and decreases isometric force of mouse muscles.
| العنوان: | Methocarbamol blocks muscular Na |
|---|---|
| المؤلفون: | Zhang, Yaxin, Otto, Philipp, Qin, Lu, Eiber, Nane, Hashemolhosseini, Said, Kröger, Stephan, Brinkmeier, Heinrich |
| المصدر: | Muscle & Nerve; Jan2021, Vol. 63 Issue 1, p141-150, 10p |
| مستخلص: | Background: The muscle relaxant methocarbamol is widely used for the treatment of muscle spasms and pain syndromes. To elucidate molecular mechanisms of its action, we studied its influence on neuromuscular transmission, on isometric muscle force, and on voltage‐gated Na+ channels. Methods: Neuromuscular transmission was investigated in murine diaphragm‐phrenic nerve preparations and muscle force studied on mouse soleus muscles. Nav1.4 channels and Nav1.7 channels were functionally expressed in eukaryotic cell lines. Results: Methocarbamol, at 2 mM, decreased the decay of endplate currents, slowed the decay of endplate potentials and reduced tetanic force of soleus muscles. The drug reversibly inhibited current flow through muscular Nav1.4 channels, while neuronal Nav1.7 channels were unaffected. Conclusions: The study provides evidence for peripheral actions of methocarbamol on skeletal muscle. Muscular Na+ channels are a molecular target of methocarbamol. Since Nav1.7 currents were unaffected, methocarbamol is unlikely to exert its analgesic effect by directly blocking Nav1.7 channels. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: | Complementary Index |
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