The onset and development of distortion product otoacoustic emissions
(DPE) representing cochlear amplifier activity were studied in neonata
l hyperthyroid (n = 10) and control (n = 10) rat pups. These were comp
ared to the onset and development of auditory nerve-brainstem evoked r
esponses (ABR) representing overall cochlear function, and to morpholo
gical development of the ear. DPEs were recorded at an earlier postnat
al age to high (8 kHz) frequencies and progressed to lower (3 kHz) fre
quencies with age. ABRs to high-intensity clicks were recorded at leas
t 2 days before DPEs, although DPE onset at 8 kHz preceded adult-like
ABR thresholds. Both ABR and DPEs appeared earlier in the hyperthyroid
rats. Histological evidence showed earlier morphological development
of the ear in these animals. ABR thresholds and DPE amplitudes matured
at a slower rate in the experimental group despite their earlier onse
t. There was no difference in ABR and DPE thresholds between adult hyp
erthyroid and control rats. However, in the experimental group, DPEs h
ad smaller amplitudes to high (70 dB SPL) and to low (50 dB SPL) stimu
lus intensities at low frequencies. Hence, despite thyroxine-injected
rat pups having earlier onset of auditory structure and function (lowe
r ABR thresholds and earlier functioning active cochlear amplifier), i
t appeared that neonatal hyperthyroidism affected the later state of t
he cochlea, such that DPEs, especially to low-frequency stimuli, were
depressed during and after maturation.