Abstract
Slow action potentials were evoked in twitch fibres of rat extensor digitorum longus (e.d.l.) and soleus muscles after drastically reducing the Cl and K conductances of the muscle fibres. Cl conductance was eliminated by exposing the muscles to a Cl-free saline in which methanesulphonate 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. In contrast, 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 first evoked response was sustained in about 60% of the fibres 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 fibres 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 microM). Tetrodotoxin did not affect the responses. These results strongly suggest that 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.