Dataset Information

Auditory white noise exposure results in intrinsic cortical excitability changes.

ABSTRACT: Cortical excitability is commonly measured by applying magnetic stimulation in combination with measuring behavioral response. This measure has, however, some shortcomings including spatial limitation to the primary motor cortex and not accounting for intrinsic excitability fluctuations. Here, we use a measure for intrinsic excitability based on phase synchronization previously validated for epilepsy. We apply this measure in 30 healthy participants' magnetoencephalography (MEG) recordings during the exposure of auditory white noise, a stimulus that has been suggested to modify cortical excitability. Using cortical parcellation of the MEG source data, we could find a specific pattern of increased and decreased excitability while participants are exposed to white noise vs. silence. Specifically, excitability during white noise exposure decreases in the frontal lobe and increases in the temporal lobe. This study thus adds to the understanding of cortical excitability changes due to specific environmental stimuli as well as the spatial extent of these effects.

SUBMITTER: Schuler AL

PROVIDER: S-EPMC10415920 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature

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Auditory white noise exposure results in intrinsic cortical excitability changes.

Schuler Anna-Lisa AL Brkić Diandra D Ferrazzi Giulio G Arcara Giorgio G Marinazzo Daniele D Pellegrino Giovanni G

iScience 20230717 8

Cortical excitability is commonly measured by applying magnetic stimulation in combination with measuring behavioral response. This measure has, however, some shortcomings including spatial limitation to the primary motor cortex and not accounting for intrinsic excitability fluctuations. Here, we use a measure for intrinsic excitability based on phase synchronization previously validated for epilepsy. We apply this measure in 30 healthy participants' magnetoencephalography (MEG) recordings durin ...[more]

PMID: 37575186

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Project description:Noise that is capable of inducing the hearing loss (NIHL) has a strong impact on the inner ear structures and causes early and most obvious pathophysiological changes in the auditory periphery. Several studies indicated that intrinsic apoptotic cell death mechanisms are the key factors inducing cellular degeneration immediately after noise exposure and are maintained for days or even weeks. In addition, studies demonstrated several changes in the central auditory system following noise exposure, consistent with early apoptosis-related pathologies. To clarify the underlying mechanisms, the present study focused on the noise-induced gene and protein expression of the pro-apoptotic protease activating factor-1 (APAF1) and the anti-apoptotic B-cell lymphoma 2 related protein a1a (BCL2A1A) in the cochlear nucleus (CN), inferior colliculus (IC) and auditory cortex (AC) of the murine central auditory pathway. The expression of Bcl2a1a mRNA was upregulated immediately after trauma in all tissues investigated, whereas the protein levels were significantly reduced at least in the auditory brainstem. Conversely, acute noise has decreased the expression of Apaf1 gene along the auditory pathway. The changes in APAF1 protein level were not statistically significant. It is tempting to speculate that the acoustic overstimulation leads to mitochondrial dysfunction and induction of apoptosis by regulation of proapoptotic and antiapoptotic proteins. The inverse expression pattern on the mRNA level of both genes might reflect a protective response to decrease cellular damage. Our results indicate the immediate presence of intrinsic apoptosis following noise trauma. This, in turn, may significantly contribute to the development of central structural deficits. Auditory pathway-specific inhibition of intrinsic apoptosis could be a therapeutic approach for the treatment of acute (noise-induced) hearing loss to prevent irreversible neuronal injury in auditory brain structures and to avoid profound deficits in complex auditory processing.

Project description:Purpose Complaints of auditory perceptual deficits, such as tinnitus and difficulty understanding speech in background noise, among individuals with clinically normal audiograms present a perplexing problem for audiologists. One potential explanation for these "hidden" auditory deficits is loss of the synaptic connections between the inner hair cells and their afferent auditory nerve fiber targets, a condition that has been termed cochlear synaptopathy. In animal models, cochlear synaptopathy can occur due to aging or exposure to noise or ototoxic drugs and is associated with reduced auditory brainstem response (ABR) wave I amplitudes. Decreased ABR wave I amplitudes have been demonstrated among young military Veterans and non-Veterans with a history of firearm use, suggesting that humans may also experience noise-induced synaptopathy. However, the downstream consequences of synaptopathy are unclear. Method To investigate how noise-induced reductions in wave I amplitude impact the central auditory system, the ABR, the middle latency response (MLR), and the late latency response (LLR) were measured in 65 young Veterans and non-Veterans with normal audiograms. Results In response to a click stimulus, the MLR was weaker for Veterans compared to non-Veterans, but the LLR was not reduced. In addition, low ABR wave I amplitudes were associated with a reduced MLR, but with an increased LLR. Notably, Veterans reporting tinnitus showed the largest mean LLRs. Conclusions These findings indicate that decreased peripheral auditory input leads to compensatory gain in the central auditory system, even among individuals with normal audiograms, and may impact auditory perception. This pattern of reduced MLR, but not LLR, was observed among Veterans even after statistical adjustment for sex and distortion product otoacoustic emission differences, suggesting that synaptic loss plays a role in the observed central gain. Supplemental Material https://doi.org/10.23641/asha.11977854.

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Auditory white noise exposure results in intrinsic cortical excitability changes.

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Auditory white noise exposure results in intrinsic cortical excitability changes.

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