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Pharmacological evidence that endogenous ATP modulates cochlear mechanics
R A Skellett1, C Chen, M Fallon
1Department of Otorhinolaryngology and Biocommunication, Louisiana State University Medical Center, New Orleans 70112-2234, USA.
Hearing Research
|November 5, 1997
Summary
Endogenous adenosine triphosphate (ATP) influences cochlear mechanics. ATP antagonists like suramin affect outer hair cell (OHC) function and distortion product otoacoustic emissions (DPOAEs), suggesting ATP
Area of Science:
- Auditory Neuroscience
- Cell Physiology
- Bioacoustics
Background:
- Outer hair cells (OHCs) and Deiters' cells are crucial for active cochlear mechanics.
- Adenosine triphosphate (ATP) receptors on these cells suggest a role for endogenous ATP in hearing.
- Understanding ATP's role is key to deciphering cochlear function and dysfunction.
Purpose of the Study:
- To investigate the role of endogenous ATP in active cochlear mechanics.
- To examine the effects of ATP antagonists on OHCs, Deiters' cells, and DPOAEs.
Main Methods:
- In vivo studies using distortion product otoacoustic emissions (DPOAEs) with cochlear perfusion.
- In vitro studies on isolated OHCs and Deiters' cells using patch-clamp techniques.
- Application of ATP and ATP antagonists (suramin, cibacron) to assess cellular and physiological responses.
Main Results:
- Extracellular ATP induced inward currents in OHCs and Deiters' cells, inhibited by suramin and cibacron.
- Cibacron modulated voltage-gated currents in OHCs and Deiters' cells differently.
- Suramin reversibly suppressed the 'slow decline' in DPOAEs, indicating an effect on active cochlear mechanics.
Conclusions:
- Endogenous ATP plays a significant role in modulating active cochlear mechanics.
- ATP antagonists, particularly suramin, can alter cochlear responses, offering potential therapeutic targets.
- These findings provide insights into the complex mechanisms of hearing.
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