Bilirubin encephalopathy results from the entry of bilirubin into the brain and is expressed by motor, sensory, and/or behavioral impairment. The jaundiced (jj) Gunn rat is a valuable animal model for studying the kinetics of bilirubin-induced neurotoxicity. This is often done by recording evoked potentials, which are also used as indices of brain damage in infants who develop neonatal jaundice, as is the case with the auditory nerve and brainstem evoked response (ABR). The present study describes the postnatal development of the somatosensory evoked potential (SEP) in Gunn rats. No effects of jaundice on the SEP were found in young jj rats (16-28 d). However, adult (3-4 mo) jj rats had prolonged latencies and decreased amplitudes of the P2 component of the SEP compared with adult nonjaundiced (Jj) rats. These changes in the SEP of jaundiced rats may reflect a synaptic lesion in these animals, possibly due to cumulative and/or progressive damage induced by bilirubin during the first 3 mo of life. After sulfadimethoxine administration, marked latency prolongations (2-6%) were observed in the early components of SEP in young (3-wk-old) jj (but not Jj) rats, as early as 2 h after injection. These changes, which became more severe (4-10%) with time, seem to be mostly peripheral. The present results suggest that the SEP may be a sensitive marker for the massive entry of bilirubin into the nervous system, and could serve as part of an evoked potential battery (in addition to visual evoked potential and ABR) in assessing bilirubin-induced neurotoxicity in jaundiced newborns and infants.