The effect of electroconvulsive shock (ECS) on the cortical somatosensory evoked potential (SEP) was studied in 25 male rats. SEPs were recorded after stimulation of the contralateral forepaw. Animals were curarized and artificially ventilated but not anesthetized. The magnitude of the ECS was 80 mA for 600 ms which produced tonic-clonic convulsions lasting an average 54 s in noncurarized control animals. SEPs were recorded during the ictal period and then at intervals for 20 min. ECS initially caused the total abolition of all components of the SEP implying a significant but transient effect on activity propagated in specific and also possibly diffuse somatosensory pathways. The reappearance of the SEP coincided with the cessation of convulsive movements and the return of the corneal reflex. The return of the waveform to near baseline condition corresponded to the regaining of the righting reflex at approximately 3 min in the control animals. The most persisting change in the SEP waveform was in the shape of the late high-amplitude component (N2) which may reflect activity in the reticular formation. Following ECS, N2 reappeared with a peak latency notably decreased (approximately 1 ms) in comparison with the mean baseline recording. There was also an attenuation in the amplitude of N2 which remained significantly depressed (at less than 50% of mean baseline amplitude) throughout the post-ECS recording period. The results are compared with the relatively few studies of the acute effects of ECS on evoked potentials in psychiatric patients and also with a neuroendocrine theory which argues that the principal site and mode of action of ECS lies in the diencephalon.