RESUMO
Studies in man have proposed that individuals with adrenocorticoid insufficiency show a heightened auditory detection threshold. This hyperacuity was shown to be specific for deficits in carbohydrate-active steroids, with threshold levels improved at least 13 dB between 1,000 Hz and 4,000 Hz. These reversible changes in auditory detection have been related to specific influences of glucocorticoids on the metabolism of neural tissue. The present study was designed to examine the hypothesis that glucocorticoid deficiencies cause decreased electrocochleographically measured auditory thresholds with interference in the central conduction of these impulses. A rat model was employed in an attempt to demonstrate the mechanism for a state of increased neural excitability in the absence of carbohydrate-active steroid influence. Electrocochleographic and auditory brain-stem evoked response threshold and latency determinations were made in eight experimental rats. Adrenalectomies were then performed in all animals with postoperative electrocochleographic and auditory brain stem responses being made at 3, 7, and 21 days. Threshold recordings for all experimental animals showed no significant changes following the cessation of glucocorticoid production. Latency measurements revealed impaired central neural transmission of the first and second order neurons. The possible mechanisms for these findings are discussed.
