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<p>Noise-induced hearing loss (NIHL) is a sensorineural disorder that provokes complex neuroplastic and neurodegenerative changes within the central nervous system (CNS). This study investigated the temporal dynamics of neuronal density, axonal integrity and glutamatergic and GABAergic neurotransmission in the central inferior colliculus (CIC) and the ventral medial geniculate body of the thalamus (MGV) after NIHL. To achieve this, a correlative multimodal approach combining audiometric, magnetic resonance imaging (MRI) and histological biomarkers was performed. Adult mice were noise-exposed to broadband white noise (5–20&#xa0;kHz) for 3&#xa0;h at either high (115&#xa0;dB SPL) or moderate (90&#xa0;dB SPL) intensity, while unexposed mice served as controls. Separate cohorts of mice were investigated 1, 7, 56 and 84&#xa0;days post-exposure using in vivo magnetic resonance imaging (MRI) techniques: Voxel-based morphometry (VBM) of gray matter density (GMD), diffusion MRI (dMRI) of microstructural connectivity, and proton magnetic resonance spectroscopy (1H-MRS) for glutamate and GABA quantification. Frequency-specific auditory brainstem responses (ABR) were recorded at 4, 8, 16 and 32&#xa0;kHz before and after exposure to examine hearing threshold (HT) shifts. Brains were subsequently processed for fluorescence immunohistochemistry (FIHC) targeting NeuN, DAPI, NF, VGAT, VGLUT1 and VGLUT2. Mice exposed to 115&#xa0;dB exhibited sustained HT elevations up to 84&#xa0;days, suggesting a NIHL phenotype. Neurofilament (NF) expression significantly increased in the CIC and MGV 1d after 115&#xa0;dB noise exposure, suggesting early axonal stress followed by normalization. dMRI alterations were observed 7d after 90&#xa0;dB noise exposure. Glutamate and GABA decreases 84d after 90&#xa0;dB exposure were also detected by 1H-MRS. No consistent changes in GMD or neuronal density were observed. Correlation analyses revealed weak relationships across audiometric, MRI and histological parameters. Overall, these findings reveal rapid neuroplastic adaptations following NIHL, and underscore the need for more sensitive biomarkers to detect early CNS consequences of NIHL.</p>

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Temporal dynamics of neuroplasticity and neurodegeneration in the central auditory system following noise-induced hearing loss: a multimodal imaging and histological study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月2日

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  • Víctor Giménez-Esbrí,
  • Susanne Schwitzer,
  • Susanne Mueller,
  • Stefan Koch,
  • Marco Foddis,
  • Stefan Donat,
  • Jan Schmoranzer,
  • Niclas Gimber,
  • Janina Zeqiraj,
  • Dietmar Basta,
  • Philipp Boehm-Sturm,
  • Moritz Gröschel

摘要

Noise-induced hearing loss (NIHL) is a sensorineural disorder that provokes complex neuroplastic and neurodegenerative changes within the central nervous system (CNS). This study investigated the temporal dynamics of neuronal density, axonal integrity and glutamatergic and GABAergic neurotransmission in the central inferior colliculus (CIC) and the ventral medial geniculate body of the thalamus (MGV) after NIHL. To achieve this, a correlative multimodal approach combining audiometric, magnetic resonance imaging (MRI) and histological biomarkers was performed. Adult mice were noise-exposed to broadband white noise (5–20 kHz) for 3 h at either high (115 dB SPL) or moderate (90 dB SPL) intensity, while unexposed mice served as controls. Separate cohorts of mice were investigated 1, 7, 56 and 84 days post-exposure using in vivo magnetic resonance imaging (MRI) techniques: Voxel-based morphometry (VBM) of gray matter density (GMD), diffusion MRI (dMRI) of microstructural connectivity, and proton magnetic resonance spectroscopy (1H-MRS) for glutamate and GABA quantification. Frequency-specific auditory brainstem responses (ABR) were recorded at 4, 8, 16 and 32 kHz before and after exposure to examine hearing threshold (HT) shifts. Brains were subsequently processed for fluorescence immunohistochemistry (FIHC) targeting NeuN, DAPI, NF, VGAT, VGLUT1 and VGLUT2. Mice exposed to 115 dB exhibited sustained HT elevations up to 84 days, suggesting a NIHL phenotype. Neurofilament (NF) expression significantly increased in the CIC and MGV 1d after 115 dB noise exposure, suggesting early axonal stress followed by normalization. dMRI alterations were observed 7d after 90 dB noise exposure. Glutamate and GABA decreases 84d after 90 dB exposure were also detected by 1H-MRS. No consistent changes in GMD or neuronal density were observed. Correlation analyses revealed weak relationships across audiometric, MRI and histological parameters. Overall, these findings reveal rapid neuroplastic adaptations following NIHL, and underscore the need for more sensitive biomarkers to detect early CNS consequences of NIHL.