AI Article Synopsis

  • Voltage-gated Ca channels (VGCCs), particularly T-type Ca3.2, are crucial for hearing and auditory processing in the inner ear and brainstem.
  • Pharmacological targeting of LVA T-type Ca channels may help treat age- and noise-related hearing loss, demonstrating their potential in managing auditory impairment.
  • Research shows that Ca3.2 channels significantly affect hearing thresholds and auditory response characteristics in mice, highlighting their essential role in auditory function and suggesting new avenues for treatment development.

Article Abstract

Voltage-gated Ca channels (VGCCs) play key roles in auditory perception and information processing within the inner ear and brainstem. Pharmacological inhibition of low voltage-activated (LVA) T-type Ca channels is related to both age- and noise induced hearing loss in experimental animals and may represent a promising approach to the treatment of auditory impairment of various etiologies. Within the LVA Ca channel subgroup, Ca3.2 is the most prominently expressed T-type channel entity in the cochlea and auditory brainstem. Thus, we performed a complete gender specific click and tone burst based auditory brainstem response (ABR) analysis of Ca3.2 and Ca3.2 mice, including i.a. temporal progression in hearing loss, amplitude growth function and wave latency analysis as well as a cochlear qPCR based evaluation of other VGCCs transcripts. Our results, based on a self-programmed automated wavelet approach, demonstrate that both heterozygous and Ca3.2 null mutant mice exhibit age-dependent increases in hearing thresholds at 5 months of age. In addition, complex alterations in W amplitudes and latencies were detected that were not attributable to alterations in the expression of other VGCCs in the auditory tract. Our results clearly demonstrate the important physiological role of Ca3.2 VGCCs in the spatiotemporal organization of auditory processing in young adult mice and suggest potential pharmacological targets for interventions in the future.

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http://dx.doi.org/10.1016/j.neuroscience.2019.04.024DOI Listing

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