Auditory evoked potential recordings were done on 14 normal subjects during baseline conditions as well as after oral administration of 0.2 mg of clonidine or placebo. P300 amplitude and latency measurements were obtained from 28 electrodes and analyzed. Clonidine resulted in a decrease in P300 amplitude, which was most marked in the occipital and left parieto-temporal regions. This effect was significant even after controlling for the sedative side effect of clonidine. P300 was unaffected by clonidine. These data suggest the possible use of clonidine-induced changes in P300 amplitude as an index of central noradrenergic responsiveness.