The early deficits of neurotoxicity induced by acrylamide were examined in rats by comparing nerve and muscle action potentials before and 24 hr after exposure to acrylamide (25, 50 or 100 mg/kg). No changes were seen in the nerve action potential amplitude or duration. The 25 mg/kg dose produced a more variable nerve conduction velocity. There was also a significant broadening of the muscle compound action potential. Neither of these effects were seen in the fasted controls. However, the lengthening of the relative refractory period of the muscle action potential was highly correlated with losses in body weight in the treatment groups and was identical to changes seen in control animals which were fasted for 24 hr. The slowed conduction of the muscle action potential may be a precursor of the nerve terminal damage which results from chronic exposure. Changes in the muscle refractory period, on the other hand, appear to be secondary to the loss in body weight which accompanies acrylamide administration.