Gating of hair cell Ca2+channels governs the activity of cochlear neurons

preprint OA: gold CC-BY-NC-ND-4.0
📄 Open PDF Full text JSON View at publisher
AI-generated deep summary by claude@2026-07, 2026-07-06 · read from full text

The paper investigates how the gating properties of Ca2+ channels in mouse inner hair cells influence neurotransmitter release onto postsynaptic spiral ganglion neurons, thereby shaping firing patterns across sound intensities. Using low-voltage activation and a mouse model carrying the human CaV1.3 A749G mutation (CaV1.3A749G/A749G), the authors report increased spontaneous SGN firing and reduced sound thresholds, along with altered synaptic morphology even at ambient sound levels. A key caveat noted is that synaptic changes were observed under standard mouse husbandry conditions, implying potential vulnerability but not directly establishing long-term noise exposure effects. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Our sense of hearing processes sound intensities spanning six orders of magnitude. In the ear, postsynaptic spiral ganglion neurons (SGNs) tile this intensity range with their firing rate codes. Presynaptic inner hair cells (IHCs) vary Ca 2+ -influx among their active zones (AZs) diversifying glutamate release and likely contributing to SGN firing diversity. Here we show that low-voltage activation of IHC-Ca 2+ -influx of mice, modeling the human Ca V 1.3 A749G mutation, increases spontaneous SGN-firing and lowers sound threshold. Altered synaptic morphology in Ca V 1.3 A749G/A749G mice already at ambient sound levels of standard mouse husbandry indicates a risk for noise-induced alterations in Ca V 1.3 A749G patients. We conclude that heterogeneous voltage-dependence of Ca V 1.3 activation among IHC-AZs contributes to the diversity of SGN firing for sound intensity coding and synaptic vulnerability.
Full text 985 characters · extracted from oa-doi-fallback · click to expand
Abstract Our sense of hearing processes sound intensities spanning six orders of magnitude. In the ear, postsynaptic spiral ganglion neurons (SGNs) tile this intensity range with their firing rate codes. Presynaptic inner hair cells (IHCs) vary Ca2+-influx among their active zones (AZs) diversifying glutamate release and likely contributing to SGN firing diversity. Here we show that low-voltage activation of IHC-Ca2+-influx of mice, modeling the human CaV1.3A749G mutation, increases spontaneous SGN-firing and lowers sound threshold. Altered synaptic morphology in CaV1.3A749G/A749G mice already at ambient sound levels of standard mouse husbandry indicates a risk for noise-induced alterations in CaV1.3A749G patients. We conclude that heterogeneous voltage-dependence of CaV1.3 activation among IHC-AZs contributes to the diversity of SGN firing for sound intensity coding and synaptic vulnerability. Competing Interest Statement The authors have declared no competing interest.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2025) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.

Source provenance

europepmc
last seen: 2026-05-20T01:45:00.602351+00:00
unpaywall
last seen: 2026-05-21T05:10:58.409756+00:00
License: CC-BY-NC-ND-4.0