Chronic triethyltin exposure reduces the resting membrane potential of rat soleus muscle

Muscle weakness is a prominent component of the toxic syndrome which results from prolonged exposure to triethyltin (TET). The etiology of this phenomenon includes, in part, an alteration of acetylcholine (ACh) release from motoneurons but there are also indications that TET causes a primary myopathy. We have found that chronic exposure of rats to TET bromide (30 mg/liter of drinking water) caused a time-dependent reduction of resting membrane potentials (RMPs) recorded in situ from soleus muscle fibers. The RMPs of TET-exposed rats were significantly lower than those of control animals (5.4 mV) after four days and were further reduced by continuous TET exposure to 11.2 mV less than control on the twenty-eighth day. Three weeks after rats were withdrawn from TET RMPs were restored to control values. TeT had no effect on the frequency, amplitude or incidence of occurrence of miniature endplate potentials. Spontaneous ACh release ane its action on the postsynaptic membrane were not affected by TET, which suggests that TET reduces RMPs through an effect on muscle fibers unrelated to denervation. We propose that TET reduces RMPs by inhibiting the bioenergetic capacity of the muscle and that this myogenic toxicity is a significant factor in the development of muscle weakness following exposure.