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Protecting the auditory system with glucocorticoids

Glucocorticoids are hormones released following stress-related events and function to maintain homeostasis. Glucocorticoid receptors localize, among others, to hair cells, spiral ligament and spiral ganglion neurons. Glucocorticoid receptor-induced protection against acoustic trauma is found by i) pretreatment with glucocorticoid agonists; ii) acute restraint stress; and iii) sound conditioning. In contrast, glucocorticoid receptor antagonists exacerbate hearing loss. These findings have important clinical significance since synthetic glucocorticoids are commonly used to treat hearing loss. However, this treatment has limited success since hearing improvement is often not maintained once the treatment has ended, a fact that reduces the overall appeal for this treatment. It must be realized that despite the wide-spread use of glucocorticoids to treat hearing disorders, the molecular mechanisms underlying this treatment are not well characterized. This review will give insight into some physiological and biochemical mechanisms underlying glucocorticoid treatment for preventing hearing loss

from Hearing Research


Recruitment of Neurons and Loudness

Without Abstract

from JARO — Journal of the Association for Research in Otolaryngology

Encoding Intensity in Ventral Cochlear Nucleus Following Acoustic Trauma: Implications for Loudness Recruitment

from JARO — Journal of the Association for Research in Otolaryngology

Abstract Loudness recruitment, an abnormally rapid growth of perceived loudness with sound level, is a common symptom of sensorineural hearing loss. Following acoustic trauma, auditory-nerve rate responses are reduced, and rate grows more slowly with sound level, which seems inconsistent with recruitment (Heinz et al., J. Assoc. Res. Otolaryngol. 6:91–105, 2005). However, rate-level functions (RLFs) in the central nervous system may increase in either slope or saturation value following trauma (e.g., Salvi et al., Hear. Res. 147:261–274, 2000), suggesting that recruitment may arise from central changes. In this paper, we studied RLFs of neurons in ventral cochlear nucleus (VCN) of the cat after acoustic trauma. Trauma did not change the general properties of VCN neurons, and the usual VCN functional classifications remained valid (chopper, primary-like, onset, etc.). After trauma, non-primary-like neurons, most noticeably choppers, exhibited elevated maximum discharge rates and steeper RLFs for frequencies at and near best frequency (BF). Primary-like neurons showed the opposite changes. To relate the neurons’ responses to recruitment, rate-balance functions were computed; these show the sound level required to give equal rates in a normal and a traumatized ear and are analogous to loudness balance functions that show the sound levels giving equal perceptual loudness in the two ears of a monaurally hearing-impaired person. The rate-balance functions showed recruitment-like steepening of their slopes in non-primary-like neurons in all conditions. However, primary-like neurons showed recruitment-like behavior only when rates were summated across neurons of all BFs. These results suggest that the non-primary-like, especially chopper, neurons may be the most peripheral site of the physiological changes in the brain that underlie recruitment.