Prenatal exposure to excessive glucocorticoids alters the programming of the metabolic and endocrine balance of various organs, including the nervous system. In the present study, prenatal glucocorticoid treatment was shown to increase the susceptibility of the inner ear to acoustic noise trauma in adult life. Acute auditory brainstem response thresholds were not different between the age-matched groups. However, when measured at 48 h and 4 weeks postexposure, the dexamethasone (DEX)-treated rats showed little or no recovery from the trauma. In contrast, normal rats showed a significant amount of recovery by 48 h postexposure and continued to show further recovery over 4 weeks. In addition, acoustic trauma resulted in a massive outer hair cell loss in the DEX rats compared to minor loss in the normal rats. To determine whether oxidative stress plays a role in the recovery phase of acoustic trauma, the free radical scavenger PBN (100 mg/kg) was administered before, during and several times after noise exposure. PBN treatment significantly reduced the physiological and morphological cochlear differences which were observed between DEX and control rats after acoustic trauma. These data support the hypothesis that alterations in the intrauterine environment may modify the developmental programme of the cochlea, inducing dysfunction later in adult life. Excessive prenatal exposure to dexamethasone decreased the potential for recovery of the cochlea to oxidative stress induced by acoustic trauma; this decreased recovery potential can be counteracted by treatment with antioxidants.

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CBA mice were sacrificed at different ages of developments at embryonic day 13 (E13), E14, E16, E19, E20 and postnatal day 1 (P1), P2, P3, P4, P6, P8, P10, P14, P16, P18, P20 and P30. The temporal bones were quickly removed and deep frozen in order to prepare cryosections for immunohistochemical staining with polyclonal antibodies against glucocorticoid receptors. The avidin-biotin, ABC-method was used to visualize binding. Both the vestibular and the cochlear regions of the inner ear were analysed. A faint staining of the crista ampullaris, the utricle and the cochlear duct was seen at E19; and staining became clearly visible at P1. A decrease in labelling was found at day 2-5 post partum whereafter an increased staining was again noticed until postnatal day 14 when an adult pattern was observed. The appearance of glucocorticoid receptors in the inner ear during development does not follow a linear curve. Further, the labelling pattern may indicate an impact of glucocorticoid receptors on the embryologic maturation itself as well as a functional role in the adult ear.

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