Small Arms Fire-like noise: Effects on Hearing Loss, Gap Detection and the Influence of Preventive Treatment

Abstract

A noise-induced loss of inner hair cell (IHC) - auditory nerve synaptic connections has been suggested as a factor that can trigger the progression of maladaptive plastic changes leading to noise-induced tinnitus. The present study used a military relevant small arms fire (SAF)-like noise (50 biphasic impulses over 2.5 min at 152 dB SPL given unilaterally to the right ear) to induce loss (∼1/3) of IHC synaptic ribbons (associated with synapse loss) in rat cochleae with only minor (less than 10%) loss of outer hair cells. Approximately half of the noise-exposed rats showed poorer Gap Detection post-noise, a behavioral indication suggesting the presence of tinnitus. There was significantly greater loss of IHC ribbons in noise-exposed rats with reduced Gap Detection compared to noise-exposed rats retaining normal Gap Detection. We have previously shown systemic administration of piribedil, memantine, and/or ACEMg significantly reduced loss of IHC ribbons induced by a 3 h 4 kHz octave band 117 dB (SPL) noise. The present study examined if this treatment would also reduce ribbon loss from the SAF-like noise exposure and if this would prevent the reduced Gap Detection. As in the previous study, piribedil, memantine, and ACEMg treatment significantly reduced the noise-induced loss of ribbons, such that it was no longer significantly different from normal. However, it did not prevent development of the reduced Gap Detection indication of tinnitus in all treated noise-exposed rats, reducing the incidence but not reaching significance.

Effects of noise exposure on auditory brainstem response and speech-in-noise tasks: a review of the literature

“…Noise-induced cochlear synaptopathy has been observed across diverse animal models including mice (Kujawa and Liberman 2009;Wang and Ren 2012;Fernandez et al 2015), guinea pigs (Lin et al 2011;Furman, Kujawa, and Liberman 2013), chinchillas (Hickman et al 2018), rats (Altschuler et al 2018) and nonhuman primates (Valero et al 2017). These exposures typically employ a short-term noise exposure, with rodent subjects typically exposed to octave band noise for two-hours.…”

Evaluation of hidden hearing loss in normal-hearing firearm users

“…Such an injury is a largely artificial condition relative to human participants who, by contrast, have a lifetime of accumulated effects of noise, age, and toxin exposures (Wu et al, 2021). However, data from impulse noise paradigms may provide an opportunity to address questions of noise-induced cochlear synaptopathy risk relative to humans, given that impulse noise has been shown to induce cochlear synaptopathy in rodent models (Altschuler et al, 2019), and impulse noise from firearm discharge could induce cochlear pathology from even a single, unprotected (or under-protected) exposure to firearm noise. Indeed, one human population in which noise-induced cochlear synaptopathy has been interpreted as being both present and permanent is firearm users, as suggested in the work by Bramhall et al (2017).…”

Temporal Alterations to Central Auditory Processing without Synaptopathy after Lifetime Exposure to Environmental Noise

“…The main phenotype (and definition) of synaptopathy is a loss of synapses between the IHCs and spiral ganglion neurons (Kobel et al 2017). Several studies have demonstrated synaptopathy in rat models (Singer et al 2013;Altschuler et al 2016Altschuler et al , 2019Hickox et al 2017), including the Sprague-Dawley strain. However, we observed no such loss of synapses at any cochlea location in our animals exposed to noise for 6 or 18 months (Fig.…”