ArticleScientific reports2024
Noise-induced hearing loss alters potassium-chloride cotransporter KCC2 and GABA inhibition in the auditory centers.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Advances in Pharmacological Approaches to Tinnitus and Hyperacusis: Insights into Mechanisms, Biomarkers, and Clinical Heterogeneity from an International Scientific Meeting.Brain sciences · 2026Article
- Time-Series Transcriptome Analysis of the Older Adult Mouse Cochlea After Noise-Induced Hearing Loss Reveals an Acute Immune Response and Recovery-Associated Pathways.Molecular neurobiology · 2025Article
- Molecular Cascades That Build and Connect Auditory Neurons from Hair Cells to the Auditory Cortex.Journal of experimental neurology · 2025Article
- Astrocytes and Tinnitus.Brain sciences · 2024Review
- Increased Risk of Sudden Sensorineural Hearing Loss in Patients Receiving Sedative-Hypnotics: A Propensity Score Weighting Cohort Study.Nature and science of sleep · 2024Article
- Protective Effects of Molecular Hydrogen on Noise-Induced Auditory and Cognitive Dysfunction.Noise & healthArticle
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Abstract
Homeostatic plasticity, the ability of neurons to maintain their averaged activity constant around a set point value, is thought to account for the central hyperactivity after hearing loss. Here, we investigated the putative role of GABAergic neurotransmission in this mechanism after a noise-induced hearing loss larger than 50 dB in high frequencies in guinea pigs. The effect of GABAergic inhibition is linked to the normal functioning of K + -Cl- co-transporter isoform 2 (KCC2) which maintains a low intracellular concentration of chloride. The expression of membrane KCC2 were investigated before and after noise trauma in the ventral and dorsal cochlear nucleus (VCN and DCN, respectively) and in the inferior colliculus (IC). Moreover, the effect of gabazine (GBZ), a GABA antagonist, was also studied on the neural activity in IC. We show that KCC2 is downregulated in VCN, DCN and IC 3 days after noise trauma, and in DCN and IC 30 days after the trauma. As expected, GBZ application in the IC of control animals resulted in an increase of spontaneous and stimulus-evoked activity. In the noise exposed animals, on the other hand, GBZ application decreased the stimulus-evoked activity in IC neurons. The functional implications of these central changes are discussed.
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