ArticleEBioMedicine2026
Perilymphatic ATP plays a critical role in modulating cochlear function to protect from loud sound induced hearing loss.
Article in EBioMedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExtracellular adenosine triphosphate (ATP) signalling via purinergic receptors plays a key role in cochlear adaptation to loud sound. Traditionally, ATP activation of purinergic receptor P2X receptors has been proposed to induce a cation shunt, reducing the endolymphatic potential and the driving force for sound transduction. However, direct evidence for this protective mechanism remains limited. Here, we provide direct experimental evidence identifying a distinct, compartment-specific ATP signalling pathway that modulates cochlear function.
methodsIn mature Dunkin-Hartley guinea pigs of either sex, we combined time-resolved confocal microscopy, electrophysiology, live-cell imaging, and fluorescence spectroscopy to characterise how compartmentalised extracellular ATP regulates cochlear function during moderate loud sound exposure.
findingsATP delivered to the perilymphatic space where P2X2 receptors localised in Reissner's membrane epithelial cells, supporting cells, and hair cells significantly reduced sound-evoked electrical potentials from 486 μV to 315 μV, outer hair cell stereocilia motion from 135 nm to 99 nm and Hensen's cell motion from 128 nm to 101 nm at 80 dB SPL. These effects were reversible upon ATP removal and accompanied by decreased intracellular calcium. In contrast, ATP applied to the endolymph produced no comparable changes. These findings demonstrate that extracellular ATP in the perilymph protects the cochlea from high-intensity sound through a mechanism distinct from the classical cation shunt model.
interpretationThese findings reveal a previously unrecognised perilymph-driven ATP signalling pathway that extend beyond the traditional P2X-mediated cation shunt, demonstrating that extracellular ATP plays a critical role in protecting the cochlea mainly from loud sound-induced hearing loss.
fundingSwedish Research Council 2017-06092 and 2022-00548.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.