1. Single units and evoked potentials were recorded in dorsal cochlear nucleus (DCN) in response to electrical stimulation of the somatosensory dorsal column and spinal trigeminal nuclei (together called MSN for medullary somatosensory nuclei) and for tactile somatosensory stimuli. Recordings were from paralyzed decerebrate cats. 2. DCN principal cells (type IV units) were strongly inhibited by electrical stimulation (single 50-μA bipolar pulse) in MSN or by somatosensory stimulation. Units recorded in the fusiform cell and deep layers of DCN were inhibited, suggesting that the inhibition affects both types of principal cells (i.e., both fusiform and giant cells). 3. Interneurons (type II units) that inhibit principal cells were only weakly inhibited by electrical stimulation and were never excited, demonstrating that the inhibitory effect on principal cells does not pass through the type II circuit. In the vicinity of the DCN/PVCN (posteroventral cochlear nucleus) boundary, units were encountered that were excited by electrical stimulation in MSN; some of these neurons responded to sound, and some did not. Their response properties are consistent with the hypothesis that they are deep- layer inhibitory interneurons conveying somatosensory information to the DCN. 4. Analysis of the evoked potentials produced by electrical stimulation in MSN suggests that the somatosensory inputs activate the granule cell system of the DCN molecular layer. A model based on previous work by Klee and Rall was used to show that the distribution of evoked potentials in DCN can be explained as resulting from radial currents produced in the DCN molecular and fusiform-cell layers by synchronous activation of granule cells inputs to fusiform and cartwheel cells. Current-source density analysis of the evoked potentials is consistent with this model. Thus molecular layer interneurons (cartwheel and stellate cells) are a second possible source of inhibition to principal cells. 5. With lower stimulus levels (20 μA) and pulse-pair stimuli (50- to 100-ms interstimulus interval), three components of the inhibitory response can be recognized in both fusiform cell layer and deep layer type IV units: a short-latency inhibition that begins before the start of the evoked potential; a longer-latency inhibition whose timing corresponds to the evoked potential; and an excitatory component that occurs on the rising phase of the evoked potential. The excitatory component is usually overwhelmed by the inhibitory components and could be derived from granule cell inputs; the long-latency inhibitory component could be derived from cartwheel cells or the hypothesized deep-layer inhibitory interneurons. The source of the short-latency inhibitory input is unknown. 6. Type IV units wore also inhibited by tactile somatosensory stimuli. The strongest effect was seen with rotation of the pinna, and most units responded weakly or not at all to touch of other parts of the body. By contrast, the largest evoked potentials were produced by stimulating at sites in MSN with receptive fields involving the vibrissae as well as the pinna. Somatosensory receptive fields of DCN neurons remain uncertain because of questions raised by surgical damage to the innervation of the head and by differences between the evoked potential and unit data. 7. Inhibition by electrical stimulation in MSN and by tactile somatosensory stimuli remained in one cat after it was deafened by injecting 3 M KCl in the cochlea. This result shows that the effects do not depend on unnoticed low-level sounds produced by touching the animal or by reflex movements produced by the electrical stimuli. 8. The effects of somatosensory inputs on the principal-cell outputs of DCN are as strong as the effects of moderate-level acoustic stimuli. Thus information about somatosensory events, including pinna motion, is necessarily present at all levels of the auditory system that receive direct or indirect inputs from DCN.