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Tamoxifen inhibits BK channels in chick cochlea without alterations in voltage-dependent activation

Mingjie Tong1, R Keith Duncan

  • 1Kresge Hearing Research Institute, Univ. of Michigan, 1150 W. Medical Center Drive, Ann Arbor, MI 48109-5616, USA.

American Journal of Physiology. Cell Physiology
|May 15, 2009
PubMed

Insights

Tamoxifen did not activate large-conductance, calcium-activated potassium (BK) channels in chicken cochlear hair cells, suggesting other molecular mechanisms are responsible for tuning frequency variations.

Area of Science:

  • Neuroscience
  • Ion Channel Physiology
  • Auditory System Research

Background:

  • Large-conductance, calcium-activated, voltage-gated potassium (BK) channels are crucial for electrical tuning in nonmammalian vertebrate hair cells.
  • Variations in BK channel kinetics along the tonotopic axis contribute to systematic changes in tuning frequency, but the underlying molecular basis is unknown.
  • Auxiliary beta(1) subunits are hypothesized to slow BK channel kinetics, influencing low-frequency tuning at the cochlear apex.

Purpose of the Study:

  • To investigate the functional presence of beta(1) subunits in chicken basilar papilla hair cells using tamoxifen (Tx) as a specific activator.
  • To determine if Tx activates BK channels in a tonotopic manner, correlating with beta(1) subunit expression.
  • To elucidate the molecular mechanisms responsible for tonotopic variations in BK channel kinetics and electrical tuning.

Main Methods:

  • Excising outside-out patches of BK channels from tall hair cells along the apical half of the chicken basilar papilla.
  • Applying tamoxifen (Tx) to assess its effect on single-channel conductance, open probability, and ensemble-averaged BK current in low- and high-density patches.
  • Analyzing BK channel activation kinetics and half-activation potential in response to Tx.

Main Results:

  • Tamoxifen (Tx) did not activate BK channels in hair cells from the cochlear apex as hypothesized.
  • Tx did not induce a tonotopic gradient in BK channel activity.
  • No significant Tx-dependent changes in BK channel activation kinetics or half-activation potential were observed.

Conclusions:

  • Electrophysiological evidence contradicts the hypothesis that beta(1) subunits mediate tamoxifen (Tx)-induced BK channel activation in the chicken basilar papilla.
  • The study suggests that molecular mechanisms independent of auxiliary beta-subunits are responsible for the tonotopic distribution of BK channel kinetics.
  • Further research is needed to identify the specific molecular players involved in generating tonotopic electrical tuning in chick hair cells.

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