© 1996 Oxford University Press
research-article |
Developmental Exposure to Aroclor 1254 Produces Low-Frequency Alterations in Adult Rat Brainstem Auditory Evoked Responses1,2
National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency Research Triangle Park, North Carolina 27711
Received January 17, 1996; accepted May 10, 1996
Developmental exposure of Long—Evans rats to 0, 1, 4, or 8 mg/kg/day Aroclor 1254 (A1254) from Gestational Day 6 through Postnatal Day 21 produces an elevated behavioral threshold for a 1-kHz tone. Brahistem auditory evoked responses (BAERs) were assessed in a subset of these animals (about 1 year old) using filtered clicks at 1 (65 and 80 dB SPL), 4 (60 and 80 dB SPL), 16 (40 and 80 dB SPL), and 32 (40 and 80 dB SPL) kHz. Aroclor 1254 decreased BAER amplitudes at 1 and 4 kHz, but not at 16 or 32 kHz. A dose-related decrease in the baseline-to-peak P1A amplitude was observed for the 1-kHz (80-dB) stimulus. Doses of 1, 4, or 8 mg/kg/day A1254 decreased the peak-to-peak amplitude of both P1AN1 and P1BN1 for a 1-kHz (80-dB) stimulus. Doses of 4 and 8 mg/kg/day A1254 decreased the peak-to-peak amplitude of N1P2 and P2N2 for a 4-kHz (60-dB) or 1-kHz (80-dB) stimulus. At 8 mg/kg/day, A1254 also increased the latency of peak P4 at 1 kHz (65 dB). The decreases in peak P1A amplitudes are consistent with a dysfunction of the cochlea and/or auditory nerve. Together, the data confirm that developmental exposure of rats to A1254 produces a permanent low- to mid-frequency auditory dysfunction and suggest a cochlear and/or auditory nerve site of action.