Exposure to Intense Noise Causes Vestibular Loss.

Mil Med. 2020 01 07;185(Suppl 1):454-461

Authors: Stewart CE, Kanicki AC, Bauer DS, Altschuler RA, King WM

Abstract
INTRODUCTION: The vestibular system is essential for normal postural control and balance. Because of their proximity to the cochlea, the otolith organs are vulnerable to noise. We previously showed that head jerks that evoke vestibular nerve activity were no longer capable of inducing a response after noise overstimulation. The present study adds a greater range of jerk intensities to determine if the response was abolished or required more intense stimulation (threshold shift).
MATERIALS AND METHODS: Vestibular short-latency evoked potential (VsEP) measurements were taken before noise exposure and compared to repeated measurements taken at specific time points for 28 days after noise exposure. Calretinin was used to identify changes in calyx-only afferents in the sacculus.
RESULTS: Results showed that more intense jerk stimuli could generate a VsEP, although it was severely attenuated relative to prenoise values. When the VsEP was evaluated 4 weeks after noise exposure, partial recovery was observed.
CONCLUSION: These data suggest that noise overstimulation, such as can occur in the military, could introduce an increased risk of imbalance that should be evaluated before returning a subject to situations that require normal agility and motion. Moreover, although there is recovery with time, some dysfunction persists for extended periods.

PMID: 32074366 [PubMed - in process]

Intense noise exposure alters peripheral vestibular structures and physiology.

J Neurophysiol. 2020 02 01;123(2):658-669

Authors: Stewart CE, Bauer DS, Kanicki AC, Altschuler RA, King WM

Abstract
The otolith organs play a critical role in detecting linear acceleration and gravity to control posture and balance. Some afferents that innervate these structures can be activated by sound and are at risk for noise overstimulation. A previous report demonstrated that noise exposure can abolish vestibular short-latency evoked potential (VsEP) responses and damage calyceal terminals. However, the stimuli that were used to elicit responses were weaker than those established in previous studies and may have been insufficient to elicit VsEP responses in noise-exposed animals. The goal of this study was to determine the effect of an established noise exposure paradigm on VsEP responses using large head-jerk stimuli to determine if noise induces a stimulus threshold shift and/or if large head-jerks are capable of evoking VsEP responses in noise-exposed rats. An additional goal is to relate these measurements to the number of calyceal terminals and hair cells present in noise-exposed vs. non-noise-exposed tissue. Exposure to intense continuous noise significantly reduced VsEP responses to large stimuli and abolished VsEP responses to small stimuli. This finding confirms that while measurable VsEP responses can be elicited from noise-lesioned rat sacculi, larger head-jerk stimuli are required, suggesting a shift in the minimum stimulus necessary to evoke the VsEP. Additionally, a reduction in labeled calyx-only afferent terminals was observed without a concomitant reduction in the overall number of calyces or hair cells. This finding supports a critical role of calretinin-expressing calyceal-only afferents in the generation of a VsEP response.NEW & NOTEWORTHY This study identifies a change in the minimum stimulus necessary to evoke vestibular short-latency evoked potential (VsEP) responses after noise-induced damage to the vestibular periphery and reduced numbers of calretinin-labeled calyx-only afferent terminals in the striolar region of the sacculus. These data suggest that a single intense noise exposure may impact synaptic function in calyx-only terminals in the striolar region of the sacculus. Reduced calretinin immunolabeling may provide insight into the mechanism underlying noise-induced changes in VsEP responses.

PMID: 31875485 [PubMed - in process]

Rapamycin but not acarbose decreases age-related loss of outer hair cells in the mouse Cochlea.

Hear Res. 2018 12;370:11-15

Authors: Altschuler RA, Kanicki A, Martin C, Kohrman DC, Miller RA

Abstract
Adding rapamycin or acarbose to diet at 9-10 months of age has been shown to significantly increase life span in both male and female UM-HET3 mice. The current study examined cochleae of male and female UM-HET3 mice at 22 months of age to determine if either treatment also influenced age-related loss of cochlear hair cells. A large loss of cochlear outer hair cells was observed at 22 months of age in untreated mice in both apical and basal halves of the cochlear spiral. Addition of acarbose to diet had no significant effect on the amount of outer hair cell loss at 22 months of age or in its pattern, with large loss in both apical and basal halves. The addition of rapamycin to diet, however, significantly reduced outer hair cell loss in the basal half of the cochlea at 22 months of age when compared to untreated mice. There was no significant difference between male and female mice in any of the conditions. Age-related outer hair cell loss in the apical cochlea precedes outer hair cell loss in the base in many mouse strains. The results of the present study suggest that rapamycin but not acarbose treatment can delay age-related loss of outer hair cells at doses at which each drug increases life span.

PMID: 30245283 [PubMed - indexed for MEDLINE]

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

Neuroscience. 2019 05 21;407:32-40

Authors: Altschuler RA, Halsey K, Kanicki A, Martin C, Prieskorn D, DeRemer S, Dolan DF

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.

PMID: 30053484 [PubMed - indexed for MEDLINE]