Glucocorticoid receptors modulate auditory sensitivity to acoustic trauma

Canlon, Barbara; Meltser, Inna; Johansson, Peter; Tahera, Yeasmin

doi:10.1016/j.heares.2006.05.009

Cited by 103 publications

(83 citation statements)

References 85 publications

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“…However, since the pathogenesis for ISSNHL is unknown, a possible effect for excessive corticosteroid in the labyrinth is difficult to predict and may even be damaging. The receptors within the labyrinth are known to up-regulate by noise stimulation and seem to influence the ear's sensitivity to acoustic trauma (30).…”

Section: Discussionmentioning

confidence: 99%

Corticosteroid Treatment of Idiopathic Sudden Sensorineural Hearing Loss

Nosrati-Zarenoe

Hultcrantz

2012

Otology &Amp; Neurotology

112

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Section: Discussionmentioning

confidence: 99%

Corticosteroid Treatment of Idiopathic Sudden Sensorineural Hearing Loss

Nosrati-Zarenoe

Hultcrantz

2012

Otology &Amp; Neurotology

112

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“…The sex difference might have been due to dynamic interactions between estrogen and prolactin or the interplay of other hormones such as cortisol, which can protect against acoustic trauma (12) and can be sex-difference sensitive in some patients with inner ear pathology (47).…”

Section: Discussionmentioning

confidence: 99%

Experimental estrogen-induced hyperprolactinemia results in bone-related hearing loss in the guinea pig

Horner¹,

Cazals²,

Guieu³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Our group (Horner KC, Guieu R, Magnan J, Chays A, Cazals Y. Neuropsychopharmacology 26: 135–138, 2002) has earlier described hyperprolactinemia in some patients presenting inner ear dysfunction. However, in that study, it was not possible to determine whether hyperprolactinemia was a cause or an effect of the symptoms. To investigate the effect of hyperprolactinemia on inner ear function, we first developed a model of hyperprolactinemia in estrogen-primed Fischer 344 rats and then performed functional studies on pigmented guinea pigs. Hyperprolactinemia induced, after 2 mo, a hearing loss of ∼30–40 dB across all frequencies, as indicated by the compound action potential audiogram. During the 3rd mo, the hearing loss continued to deteriorate. The threshold shifts were more substantial in males than in females. Observations under a dissection microscope revealed bone dysmorphology of the bulla and the cochlea. Light microscopy observations of cryostat sections confirmed bone-related pathology of the bony cochlear bulla and the cochlear wall and revealed morphopathology of the stria vascularis and spiral ligament. Scanning electron microscopy revealed loss of hair cells and stereocilia damage, in particular in the upper three cochlear turns and the two outermost hair cell rows. The data provide the first evidence of otic capsule and hair cell pathology associated with estrogen-induced prolonged hyperprolactinemia and suggest that conditions such as pregnancy, anti-psychotic drug treatment, aging, and/or stress might lead to similar ear dysfunctions.

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“…Whether tinnitus is peripheral dependent or not may depend on the cochlear residual activity and therefore on the extent of cochlear damages. One notes that the susceptibility of the cochlea to various stressors can vary as a function of the context and among individuals and species (Canlon et al 2007;Graham et al 2011;Turner et al 2005).…”

Section: Implications For Understanding Tinnitus Mechanisms and Tinnimentioning

confidence: 99%

Suppression of putative tinnitus-related activity by extra-cochlear electrical stimulation

Noreña

Mulders

Robertson

2015

Journal of Neurophysiology

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Noreña AJ, Mulders WH, Robertson D. Suppression of putative tinnitus-related activity by extra-cochlear electrical stimulation. J Neurophysiol 113: 132-143, 2015. First published October 8, 2014 doi:10.1152/jn.00580.2014.-Studies on animals have shown that noise-induced hearing loss is followed by an increase of spontaneous firing at several stages of the central auditory system. This central hyperactivity has been suggested to underpin the perception of tinnitus. It was shown that decreasing cochlear activity can abolish the noise-induced central hyperactivity. This latter result further suggests that an approach consisting of reducing cochlear activity may provide a therapeutic avenue for tinnitus. In this context, extra-cochlear electric stimulation (ECES) may be a good candidate to modulate cochlear activity and suppress tinnitus. Indeed, it has been shown that a positive current applied at the round window reduces cochlear nerve activity and can suppress tinnitus reliably in tinnitus subjects. The present study investigates whether ECES with a positive current can abolish the noise-induced central hyperactivity, i.e., the putative tinnitus-related activity. Spontaneous and stimulus-evoked neural activity before, during and after ECES was assessed from single-unit recordings in the inferior colliculus of anesthetized guinea pigs. We found that ECES with positive current significantly decreases the spontaneous firing rate of neurons with high characteristic frequencies, whereas negative current produces the opposite effect. The effects of the ECES are absent or even reversed for neurons with low characteristic frequencies. Importantly, ECES with positive current had only a marginal effect on thresholds and tone-induced activity of collicular neurons, suggesting that the main action of positive current is to modulate the spontaneous firing. Overall, cochlear electrical stimulation may be a viable approach for suppressing some forms of (peripheral-dependent) tinnitus.

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Glucocorticoid receptors modulate auditory sensitivity to acoustic trauma

Cited by 103 publications

References 85 publications

Corticosteroid Treatment of Idiopathic Sudden Sensorineural Hearing Loss

Corticosteroid Treatment of Idiopathic Sudden Sensorineural Hearing Loss

Experimental estrogen-induced hyperprolactinemia results in bone-related hearing loss in the guinea pig

Suppression of putative tinnitus-related activity by extra-cochlear electrical stimulation

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