Arachidonic acid-induced activation of large-conductance potassium channels and membrane hyperpolarization in mouse B

Haifeng Zheng1, Joo Hyun Nam, Yen Hoang Nguen

  • 1Department of Physiology, Seoul National University College of Medicine, 28 Yongon-dong, Chongro-gu, Seoul, 110-799, South Korea.

Insights

Arachidonic acid (AA) activates large-conductance background K(+) channels (LK(bg)) in immature B cells, inhibiting other K(+) channels. This LK(bg) activation may influence immature B cell responses to AA.

Area of Science:

  • Immunology
  • Cell Physiology
  • Molecular Biology

Background:

  • Lymphocytes utilize voltage-gated (Kv) and Ca(2+)-activated (IKCa1) K(+) channels.
  • Immature B cells (WEHI-231) express unique voltage-independent K(+) channels, termed large-conductance background K(+) channels (LK(bg)).
  • Arachidonic acid (AA) is implicated in regulating immature B cell apoptosis.

Purpose of the Study:

  • To investigate the functional targets of AA in B cells.
  • To elucidate the effects of AA on membrane currents, voltages, and intracellular calcium concentrations ([Ca(2+)](c)) in immature (WEHI-231) and mature (Bal-17) mouse B cells.

Main Methods:

  • Whole-cell and inside-out patch clamp electrophysiology.
  • Fura-2 spectrofluorimetry for measuring intracellular calcium.
  • Isolation of primary immature B cells from mouse spleen.

Main Results:

  • AA inhibited Kv and IKCa1 channels in both cell types.
  • AA activated LK(bg) and non-selective cationic (NSC) currents in WEHI-231 cells, and NSC currents in Bal-17 cells.
  • AA induced hyperpolarization in WEHI-231 cells and depolarization in Bal-17 cells, with distinct effects on intracellular calcium dynamics.

Conclusions:

  • Novel LK(bg) channels in immature B cells are strongly activated by AA, while common lymphocyte K(+) channels are inhibited.
  • AA-induced LK(bg) activation and subsequent hyperpolarization may play a role in immature B cell responses.
  • These findings reveal specific ionic channel modulation by AA in distinct B cell populations.

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