Prenatal cocaine exposure has been associated with a variety of adverse neurological effects in infants and laboratory animals. Of particular interest, one group of investigators reported that exposed neonates have an abnormality in the brainstem auditory-evoked potential (BAEP). The particular abnormality, a prolongation in the wave I-V interpeak latency, suggested delayed or desynchronized transmission of subcortical auditory information. To further investigate this possible consequence of prenatal cocaine exposure, pregnant Long-Evans rats were injected daily with 60, 80 or 100 mg/kg cocaine HCl (SC, 2% solution) with half the daily dose given in the morning and the other half given in the afternoon. Treatment was given from gestation days 7 to 20 (sperm positive = GD 0). Ad lib-fed and pair-fed control groups were also used. Offspring were evaluated at the age of 35 days (birth = PD 0) and as adults (6-10 months). BAEPs were elicited by click stimuli presented over a broad range of intensities and repetition rates. Prolongation of the interpeak latencies and a reduction in BAEP amplitudes were observed only in the highest dose (C100) group, only at the age of 35 days, and only at the highest stimulus intensity. While these results support those found in exposed neonates, our data suggest a) that the effects are developmental delays which dissipate with aging and b) that the effects require high cocaine exposure.