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Hair cells are the sensory receptors of the auditory system—they transduce mechanical sound waves into electrical energy that the nervous system can understand. Hair cells are located in the organ of Corti within the cochlea of the inner ear, between the basilar and tectorial membranes. The actual sensory receptors are called inner hair cells. The outer hair cells serve other functions, such as sound amplification in the cochlea, and are not discussed in detail here.

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Related Experiment Video

Updated: May 11, 2026

Spiral Ganglion Neuron Explant Culture and Electrophysiology on Multi Electrode Arrays

Spiral Ganglion Neuron Explant Culture and Electrophysiology on Multi Electrode Arrays

Published on: October 19, 2016

Active cochlear amplification is dependent on supporting cell gap junctions.

Yan Zhu¹, Chun Liang, Jin Chen

¹Department of Otolaryngology, University of Kentucky Medical School, Lexington, Kentucky 40536, USA.

Nature Communications

|May 9, 2013

Summary

This summary is machine-generated.

Supporting cell gap junctions, specifically connexin 26, are crucial for active cochlear amplification in mammals. Their deficiency impairs outer hair cell function, leading to hearing loss.

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Area of Science:

Auditory Neuroscience
Cell Biology
Physiology

Background:

Mammalian hearing depends on active cochlear mechanics for sensitivity and frequency selectivity.
Outer hair cell (OHC) electromotility and hair bundle movement are key to this process.
The role of supporting cell gap junctions in this mechanism was previously unclear.

Purpose of the Study:

To investigate the role of gap junctions between cochlear supporting cells in active cochlear amplification in vivo.
To determine the impact of connexin 26 deficiency in specific supporting cells on OHC function and hearing.

Main Methods:

Targeted deletion of connexin 26 in Deiters cells and outer pillar cells in vivo.
Assessment of outer hair cell electromotility.
Measurement of active cochlear amplification.
Evaluation of distortion product otoacoustic emissions (DPOAEs) and hearing thresholds.

Main Results:

Targeted deletion of connexin 26 in supporting cells caused a leftward shift in OHC electromotility towards hyperpolarization.
Active cochlear amplification was reduced, accompanied by a significant decrease in DPOAEs.
Severe high-frequency hearing loss was observed, with larger shifts in shorter OHCs.
Connexin 26 deficiency in supporting cells directly impacts OHC function and hearing.

Conclusions:

Active cochlear amplification in vivo is critically dependent on gap junctions between cochlear supporting cells.
Connexin 26 in these supporting cells plays a vital role in maintaining normal hearing function.
Deficiency in supporting cell connexin 26 can lead to hearing loss by impairing active cochlear amplification.