Calcium action potentials in rat fast‐twitch and slow‐twitch muscle fibres.

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Abstract
Slow action potentials were evoked in twitch fibers of rat extensor digitorum longus (e.d.l.) and soleus muscules after drastically reducing the Cl and K conductances of the muscle fibers. Cl conductance was eliminated by exposing the muscles to a Cl-free saline in which methanesulfonate replaced Cl. K conductance was reduced by adding tetraethylammonium (TEA) and 3,4-diaminopyridine (3,4-DAP) to the Cl-free saline or by overnight incubation of the muscles in a saline containing Cs and TEA. The delayed rectifier was markedly blocked by TEA and 3,4-DAP. The inward rectifier was blocked only by TEA. Depolarization with pulses of increasing amplitude triggered slow responses which had a threshold of -30 to -10 mV and a peak amplitude of 50-60 mV. In e.d.l. muscles, the time course of the response was sustained for the duration of the pulses and was not affected by repeated stimulation. In soleus muscles, the 1st evoked response was sustained in .apprx. 60% of the fibers and transient in the rest. Transient responses reached a peak amplitude and were followed by a hyperpolarization. Repeated stimulation irreversibly transformed the sustained responses of soleus fibers into transient ones. The responses were blocked when the Ca in saline was replaced by Mg (10 mM) or Co (5 mM) or by the addition of Cd (0.1-1.0 mM) or nifedipine (5-6 .mu.M). Tetrodotoxin did not affect the responses. Ca is the main carrier of current during the response. Nifedipine blocked both the Ca response and the subsequent hyperpolarization, suggesting that the latter is due to the activation of a Ca-dependent K conductance.