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Activation of large conductance background K+ channels by arachidonic acids in murine B cells

Mouse B cells express a phosphatidylinositol 4,5‐bisphosphate (PIP2)‐inhibited large conductance background K+channels (BKbg). In inside‐out membrane patches, the application of ATP inhibited BKbg due to the generation of PIP2 by PI‐kinases. The activity of BKbg is low in cell‐attached (c‐a) conditions. Generation of arachidonic acid (AA) by phospholipase A2 is involved in the apoptosis of immature B cells by antigen receptor stimulation. Some members of the cloned background K+ channels are activated by AA. Similarly, the application of AA activated BKbg of B lymphocytes in c‐a as well as in i‐o patches. The facilitating effects of fatty acids became weaker as the acyl chain is more saturated; AA > oleic acid > plamitic acid. When the activity of BKbg was strongly inhibited by a direct application of PIP2 (5 uM), the addition of AA hardly recovered BKbg activity. The facilitation of BKbg by AA was fully reversible and unaffected by the treatment with inhibitors of various metabolizing enzymes for AA. Consistent with the activation of BKbg, the application of AA induced strong hyperpolarization of membrane potential in WEHI‐231 cells. The intracellular [Ca2+] of WEHI‐231 was increased by AA, which was partly diminished by KCl‐induced membrane depolarization. AA strongly augmented the store‐operated Ca2+ entry in WEHI‐231. Besides the increase of BKbg, AA activated Ca2+ permeable nonselective cation channels. Since the expression of PLA2 is reportedly higher in immature than mature B lymphocytes, the increased driving force for Ca2+ influx by AA might play a crucial role in the regulation and development of B lymphocytes.