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Related Experiment Videos

Cyclic GMP and outer hair cell electromotility.

M Szönyi1, D Z He, O Ribári

  • 1Auditory Physiology Laboratory, Departments of Communication Sciences and Disorders and Neurobiology and Physiology, Institute for Neuroscience, Northwestern University, Evanston, IL 60208, USA.

Hearing Research
|November 5, 1999
PubMed
Summary

Outer hair cell (OHC) electromotility is modulated by cyclic guanosine monophosphate (cGMP), not by cyclic adenosine monophosphate (cAMP) or protein kinase C pathways. Dibutyryl cGMP significantly increased OHC motility, suggesting a cGMP-dependent pathway regulates this response.

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Area of Science:

  • Otoacoustic emissions research
  • Cellular physiology
  • Biophysics

Background:

  • Outer hair cells (OHCs) are crucial for hearing, exhibiting electromotility in response to electrical stimulation.
  • Understanding the signaling pathways that modulate OHC function is essential for auditory research.

Purpose of the Study:

  • To investigate the role of phosphorylation pathways in regulating the electrically evoked motility of isolated OHCs.
  • To determine if cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP) pathways influence OHC electromotility.

Main Methods:

  • Isolated guinea pig OHCs were subjected to transcellular electrical stimulation in a microchamber.
  • Motility was measured before and after the application of Forskolin (cAMP pathway activator), phorbol 12-myristate 13-acetate (PMA, protein kinase C activator), and dibutyryl cGMP (cGMP agonist).

Related Experiment Videos

  • Control experiments included L15 medium and dimethyl sulfoxide (DMSO).

    • Main Results:

    • Dimethyl sulfoxide (DMSO) alone significantly decreased OHC electromotility.
    • Forskolin and PMA did not reverse the DMSO-induced decrease in motility, indicating no modulation by cAMP-dependent protein kinase or calcium/phospholipid-dependent protein kinase.
    • Dibutyryl cGMP (DBcGMP) significantly increased electromotility magnitude.
    • The effect of DBcGMP was inhibited by a cGMP antagonist, confirming pathway specificity.

    Conclusions:

    • OHC electromotility is modulated by a cGMP-dependent pathway.
    • The cAMP and protein kinase C pathways do not appear to play a significant role in modulating OHC electromotility.
    • These findings provide insights into the molecular mechanisms underlying cochlear amplification.