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Slow Calcium Signals after Tetanic Electrical Stimulation in Skeletal Myotubes

Centro de Estudios Moleculares de la Célula, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile

Correspondence: Address reprint requests to Enrique Jaimovich, Centro de Estudios Moleculares de la Célula, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Casilla 70005, Independencia 1027, Santiago 6530499, Chile. Tel.: 562-678-6510; Fax: 562-735-3510; E-mail: ejaimovi{at}med.uchile.cl.

The fluorescent calcium signal from rat myotubes in culture was monitored after field-stimulation with tetanic protocols. After the calcium signal sensitive to ryanodine and associated to the excitation-contraction coupling, a second long-lasting calcium signal refractory to ryanodine was consistently found. The onset kinetics of this slow signal were slightly modified in nominally calcium-free medium, as were both the frequency and number of pulses during tetanus. No signal was detected in the presence of tetrodotoxin. The participation of the dihydropyridine receptor (DHPR) as the voltage sensor for this signal was assessed by treatment with agonist and antagonist dihydropyridines (Bay K 8644 and nifedipine), showing an enhanced and inhibitory response, respectively. In the dysgenic GLT cell line, which lacks the 1_S subunit of the DHPR, the signal was absent. Transfection of these cells with the 1_S subunit restored the slow signal. In myotubes, the inositol 1,4,5-trisphosphate (IP₃) mass increase induced by a tetanus protocol preceded in time the slow calcium signal. Both an IP₃ receptor blocker and a phospholipase C inhibitor (xestospongin C and U73122, respectively) dramatically inhibit this signal. Long-lasting, IP₃-generated slow calcium signals appear to be a physiological response to activity-related fluctuations in membrane potential sensed by the DHPR.

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