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Like the original cohort, E 2-treated mice displayed significantly larger wave-1 amplitudes at all frequencies examined (data not shown). Mice in the vehicle-treated condition received additional subcutaneous vehicle injections during the second week of data collection, while mice in the E 2-treated condition received subcutaneous injections of E 2. This cohort utilized a between animal design ( Figure 2A). Using an additional cohort, we quantified the number of IHC synapses in E 2-treated and vehicle-treated female mice to determine if the observed improvements in auditory thresholds and increase in wave-1 amplitudes could be the result of changes to the number of paired IHC-ANF synapses. We observed statistically significant increases in the wave-1 amplitudes at each frequency tested, particularly at the higher stimulus intensities ( Figure 1C–F). Suprathreshold wave-1 amplitudes-a measure of the synchronous neural activity at the level of the spiral ganglion-were compared before and after E 2-replacement in each animal. Following E 2-replacement, ABR thresholds improved at 24 kHz ( p = 0.0416) and 32 kHz ( p = 0.0003) ( Figure 1B).

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Following octave-band noise exposures, this loss often occurs half an octave above the noise band and in the more vulnerable basal portions of the cochlea, where basal OHCs display an intrinsic vulnerability to damage caused by free radicals compared to more apical OHCs Īuditory thresholds and wave-1 amplitudes were compared before and after E 2-replacement within the same animals. Finally, the most severe subtype of NIHL results in a permanent elevation of auditory thresholds-or permanent threshold shift (PTS)-with attendant damage to, or loss of, IHCs and OHCs.

In humans, cochlear synaptopathy is believed to underpin ‘hidden hearing loss’ (HHL), a functional impairment that includes difficulty understanding speech in noise. A more severe subtype of NIHL called cochlear synaptopathy also produces a TTS but causes uncoupling and/or dysfunction of the synaptic connections between IHCs and high-threshold, low-spontaneous rate SGNs, which appear to correspond to type-1C SGNs. The least severe subtype of NIHL-referred to as a temporary threshold shift (TTS)-results in a temporary elevation of auditory thresholds without loss of, or permanent damage to, the mechanosensory cells of the cochlea-inner hair cells (IHCs) and outer hair cells (OHCs)-or their associated auditory nerve fibers (ANFs) arising from the spiral ganglion neurons (SGNs). Small increases in the intensity or duration of a noise exposure result in the progression from a less severe to a more severe subtype. The severity of NIHL presents as a continuum. Taken together, these data indicate the estrogen signaling pathways may be harnessed for the prevention and treatment of NIHL. Lastly, using fluorescent in situ hybridization, we demonstrate co-localization of estrogen receptor-2 with type-1C, high threshold spiral ganglion neurons, suggesting that the observed protection from cochlear synaptopathy may occur through E 2-mediated preservation of these neurons. Histological analysis of the cochlear tissue revealed that E 2-replacement mitigated outer hair cell loss and cochlear synaptopathy following noise exposure compared to vehicle-treatment. E 2-replacement in gonadectomized female mice protected against hearing loss following permanent threshold shift (PTS)- and temporary threshold shift (TTS)-inducing noise exposures. Functional analysis of auditory physiology in gonadectomized female mice revealed that E 2-treatment modulated the peripheral response to sound in the absence of changes to the endocochlear potential compared to vehicle-treatment.

Here, we gonadectomized B6CBAF1/J mice and used a combination of electrophysiological and histological techniques to study the effects of estrogen replacement on peripheral auditory physiology in the absence of noise exposure and on protection from NIHL.

We hypothesize that 17β-estradiol (E 2), a known modulator of auditory physiology, may underpin sex-differences in the response to noise trauma. Recent studies have identified sex-differences in auditory physiology and in the susceptibility to noise-induced hearing loss (NIHL).