In previous studies we reported that large-amplitude inhibitory potentials were elicited in masseter motoneurons by auditory stimuli (95-dB clicks) and stimulation of the sciatic nerve in alpha-chloralose-anesthetized cats [Kohlmeier K. A. et al. (1994) Soc. Neurosci. Abstr. 20, 1218; Kohlmeier K. A. et al. (1995) Sleep Res. 24, 9]. These potentials were always elicited during motor atonia induced by the pontine injection of carbachol into the nucleus pontis oralis and were never elicited prior to atonia. In the present report, the hyperpolarizing potentials that arose in response to clicks and stimulation of the sciatic nerve were blocked following the juxtacellular application of strychnine, a glycinergic antagonist. In contrast, bicuculline, a GABA(A) receptor antagonist, did not suppress the carbachol-dependent hyperpolarizing potentials elicited by these stimuli. In some motoneurons, blockade of the inhibitory potential by strychnine revealed a depolarizing potential. These data suggest that clicks and stimulation of the sciatic nerve not only elicit inhibition of motoneurons but also activate an excitatory drive which is masked by elicited inhibitory postsynaptic potentials. These findings suggest that glycine is likely to be the neurotransmitter that is responsible for the inhibitory postsynaptic potentials elicited in masseter motoneurons following the presentation of auditory and somatosensory stimuli during carbachol-induced motor atonia. We suggest that the same system that mediates glycinergically-dependent motor atonia during naturally occurring active sleep [Chase M. H. et al. (1989) J. Neurosci. 9, 743-751] also mediates the carbachol-dependent response of motoneurons to sensory stimuli.