Functional assessment of Ca(2+)-current in the mouse motor nerve terminals.

The purpose of this study was to characterize voltage-gated Ca2+ channels on the mouse motor nerve terminals. Mouse diaphragm and triangularis sterni preparations were used for this study in order to assess the functional Ca2+ channels in the transmitter release. The results showed that omega-conotoxin MVIIC (CTx-MVIIC, 0.5-1 microM) but not omega-conotoxin GVIA (1 mM) markedly inhibits not only the nerve-evoked muscle contractions accompanied by a decrease in the amplitude of end plate potentials (epps) in the mouse phrenic-nerve diaphragm but also the Ca(2+)-waveforms in the nerve terminals of triangularis sterni. The inhibitory effects of CTx-MVIIC were considered to be specifically presynaptic rather than myogenic, since none of the electrical properties of muscle fibers including action potentials, resting membrane potentials and the miniature endplate potential, were affected. Moreover, Na(+)- and K(+)-waveforms of the nerve terminals were unaffected by CTx-MVIIC. At a saturating concentration of 3-5 mM, CTx-MVIIC exerted a maximal inhibitory effect by 38% of 3,4-diaminopyridine-prolonged epps area and inhibited only the slow component of Ca(2+)-current, respectively, and the remaining fast component could be inhibited by subsequent addition of cadmium chloride (Cd2+). All of these findings indicate that at least two components (a slow CTx-MVIIC sensitive component and a fast Cd2+ sensitive component) of the mouse motor nerve terminals would cooperate in the induction of the transmitter release from motor nerve endings.