L-type calcium channel modulation reveals the relationship between neuronal synchrony and hyperactivity in the inferior colliculus following noise-induced hearing loss.

Selin Yalcinoglu, Rod D Braun, Ammaar Wattoo, Aaron K Apawu, Rasheed Alrayashi, Avril Genene Holt

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Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

6 authors.

Selin YalcinogluOphthalmology, Visual and Anatomical Sciences, School of Medicine, Wayne State University, 550 East Canfield, Detroit, MI, 48201, USA.

Rod D BraunOphthalmology, Visual and Anatomical Sciences, School of Medicine, Wayne State University, 550 East Canfield, Detroit, MI, 48201, USA.

Ammaar WattooOphthalmology, Visual and Anatomical Sciences, School of Medicine, Wayne State University, 550 East Canfield, Detroit, MI, 48201, USA.

Aaron K ApawuDepartment of Chemistry and Biochemistry, University of Northern Colorado, Greeley, CO, 80639, USA.

Rasheed AlrayashiOphthalmology, Visual and Anatomical Sciences, School of Medicine, Wayne State University, 550 East Canfield, Detroit, MI, 48201, USA.

Avril Genene HoltOphthalmology, Visual and Anatomical Sciences, School of Medicine, Wayne State University, 550 East Canfield, Detroit, MI, 48201, USA. agholt@med.wayne.edu.

Funding

Novel Theranostic Approaches to Identify and Treat Tinnitus Using Functionalized NanoparticlesR21DC013895 · NIDCD · SUNY POLYTECHNIC INSTITUTE · PI BERGKVIST, MAGNUS · 2015 to 2016

$416k

NIDCD NIH HHS R21 DC013895RRD VA I01 RX001095

6 · The paper itself

Abstract

Previous studies have established the protective effects of calcium channel inhibition on the peripheral auditory system in response to noise exposure. While these studies implicate L-type calcium channels (LTCCs) in noise-generated dysfunction in the auditory periphery, contributions of LTCCs to noise-induced central dysfunction remains unclear. To begin to elucidate the roles of LTCCs in hearing, peripheral and central auditory function were assessed longitudinally after LTCC inhibition. Neuronal synchrony and activity were assessed by analyzing wave I (peripheral) and wave V (central) auditory brainstem responses (ABRs). Just prior to a noise exposure resulting in a temporary shift in hearing thresholds, rats were administered verapamil (LTCC blocker) or saline. Verapamil administration prevented the noise-induced decrease in ABR wave I and V amplitudes. Interestingly, when non-noise exposed animals were administered verapamil, wave V amplitude decreased, suggesting that LTCCs are critical for neuronal synchrony in the inferior colliculus. The inferior colliculus mediates gap inhibition of the acoustic startle reflex (giASR). Following noise exposure, giASR was enhanced, but the enhancement was not prevented by LTCC antagonism. These results suggest that while LTCCs are necessary for auditory-related synchronous activity, these channels do not directly contribute to noise-induced hyperactivity in the inferior colliculus.

Indexed as

Calcium Channels, L-TypeHearing Loss, Noise-InducedInferior ColliculiNeuronsAcoustic StimulationAnimalsAuditory ThresholdCalcium Channel BlockersEvoked Potentials, Auditory, Brain StemMaleNoiseRatsRats, Sprague-DawleyReflex, StartleVerapamilCalcium Channel BlockersCalcium Channels, L-TypeVerapamilABR (auditory brainstem response)Auditory systemCalcium channel blockersCochleaGap inhibition of acoustic startle reflexInferior colliculusNeuronal activityNeuroprotectionNoise-induced hearing loss

Identifiers

PMID41365985

DOI10.1038/s41598-025-29536-8

PMCPMC12770476

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.