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Endolymphatic perfusion with EGTA-acetoxymethyl ester inhibits asphyxia- and furosemide-induced decrease in

Akihito Mineharu1, Yoshiaki Mori, Yoshitsugu Nimura

  • 1Department of Physiology II and Department of Otolaryngology, Osaka Medical College, Takatsuki, Osaka, 569-8686 Japan.

The Japanese Journal of Physiology
|March 31, 2005
PubMed
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This summary is machine-generated.

Elevated calcium in endolymph (Ca(e)) decreases the endocochlear potential (EP). Intracellular calcium (Ca(i)) in cochlear cells is crucial for maintaining the EP, influencing auditory function.

Area of Science:

  • Oto-neuroscience
  • Auditory Physiology
  • Cellular Electrophysiology

Background:

  • The endocochlear potential (EP) is vital for hearing.
  • The role of calcium ions (Ca2+) in EP generation is not fully understood.
  • Investigating Ca2+ effects on EP is key to understanding auditory function.

Purpose of the Study:

  • To investigate the impact of endolymphatic calcium concentration ([Ca](e)) and intracellular calcium ([Ca](i)) on the EP.
  • To determine the contribution of Ca2+ to EP generation and maintenance.
  • To elucidate the mechanisms underlying EP regulation by Ca2+.

Main Methods:

  • Utilized endolymphatic and perilymphatic perfusion techniques in cochlear models.
  • Manipulated [Ca](e) and [Ca](i) using calcium ions and chelators (EGTA-AM).

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  • Measured EP changes induced by asphyxia, furosemide, and Ca2+ alterations.

    • Main Results:

    • Increased [Ca](e) correlated with a significant decrease in EP.
    • Endolymphatic perfusion with high Ca2+ reduced EP, suggesting stria vascularis permeability.
    • Intracellular Ca2+ chelation (EGTA-AM) increased EP and suppressed EP changes.

    Conclusions:

    • Endolymphatic Ca2+ concentration directly influences EP magnitude.
    • Intracellular Ca2+ within cochlear cells plays a critical role in generating and maintaining the EP.
    • Findings provide insights into Ca2+-dependent mechanisms of auditory transduction.