ArticleJournal of molecular neuroscience : MN2021
Characterization of EGR-1 Expression in the Auditory Cortex Following Kanamycin-Induced Hearing Loss in Mice.
Article in Journal of molecular neuroscience : MN, 2021. 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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6 citing papers in PubMed, 6 citations in OpenAlex.
- Subtype-Specific Vulnerability of Spiral Ganglion Neurons in Sensorineural Hearing Loss Across the Lifespan.Brain sciences · 2026Review
- Functional pathogenicity of ESRRB variant of uncertain significance contributes to hearing loss (DFNB35).Scientific reports · 2024Article
- A basement membrane extract-based three-dimensional culture system promotes the neuronal differentiation of cochlear Sox10-positive glial cellsMaterials today. Bio · 2024Article
- Glutathione Peroxidase 1 Protects Against Peroxynitrite-Induced Spiral Ganglion Neuron Damage Through Attenuating NF-κB Pathway Activation.Frontiers in cellular neuroscience · 2022Article
- Mechanism and Prevention of Spiral Ganglion Neuron Degeneration in the Cochlea.Frontiers in cellular neuroscience · 2021Review
- Regulation of Spiral Ganglion Neuron Regeneration as a Therapeutic Strategy in Sensorineural Hearing Loss.Frontiers in molecular neuroscience · 2021Review
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Authors and funding
11 authors at 1 institution in 1 country.
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Abstract
Deprivation of acoustic input during a critical period leads to abnormal auditory development in humans. The molecular basis underlying the susceptibility of auditory cortex to loss of afferent input remains largely unknown. The transcription factor early growth response-1 (EGR-1) expression in the visual cortex has been shown to be crucial in the formation of vision, but the role of EGR-1 during the process of auditory function formation is still unclear. In this study, we presented data showing that EGR-1 was expressed in the neurons of the primary auditory cortex (A1) in mice. We observed that the auditory deprivation induced by kanamycin during the auditory critical period leads to laminar-specific alteration of neuronal distribution and EGR-1 expression in A1. In addition, MK-801 administration inhibited the expression of EGR-1 in A1 and aggravated the abnormal cortical electric response caused by kanamycin injection. Finally, we showed that the expression of PI3K, the phosphorylation of Akt, as well as the phosphorylation of cAMP-responsive element-binding protein (CREB) were decreased in A1 after kanamycin-induced hearing loss. These results characterized the expression of EGR-1 in A1 in response to the acoustic input and suggested the involvement of EGR-1 in auditory function formation.
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