Acetylcholine-induced currents were measured in partially depolarized mouse soleus muscles, denervated for 3-6 days by using a point voltage clamp. When 0.25 microM d-tubocurarine (d-Tc) was used, the weak currents provoked by 0.1 microM ACh, at a holding potential of -20 mV, were barely affected, while the large currents provoked by 2-5 microM ACh were decreased by more than 50%. By contrast, weak and strong ACh-induced currents were proportionally diminished when, under similar conditions, 20-100 microM ipratropium was used. Currents were proportionally diminished by d-Tc when the holding potential was set at +15 mV, a level corresponding to the reversal potential of the current provoked by small concentrations of ACh. In non-denervated flexor digitorum brevis muscles, d-Tc had the same relative effect at small and at large concentrations of ACh, independent of the holding potential. The reversal potential for the ACh-induced currents was about +14 mV for small concentrations of ACh and decreased to about +3 mV with 4 microM ACh in denervated soleus muscles. It was concluded that denervated soleus muscles, in contrast to the endplate regions of non-denervated mouse muscles, contain a small proportion of highly ACh-sensitive, weakly d-Tc-sensitive, predominantly Na(+)-permeable ACh receptors. These receptors are presumably responsible for the non-fading ACh-induced currents, described before, for the denervated mouse soleus muscle.