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The Journal of Neurophysiology Vol. 81 No. 2 February 1999, pp. 611-624
Copyright ©1999 by the American Physiological Society
1Department of Anesthesiology and 2Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110
RINm5f cells express inactivating BK channels whereas HIT cells express
noninactivating BK channels. Large-conductance
Ca2+- and voltage-activated BK-type K+
channels are expressed abundantly in normal rat pancreatic islet cells
and in the clonal rat insulinoma tumor (RINm5f) and hamster insulinoma
tumor (HIT) beta cell lines. Previous work has suggested that the
Ca2+ sensitivity of BK channels in RIN cells is
substantially less than that in HIT cells, perhaps contributing
to differences between the cell lines in responsiveness to glucose in
mediating insulin secretion. In both RIN cells and normal pancreatic
beta cells, BK channels are thought to play a limited role in responses
of beta cells to secretagogues and in the electrical activity of beta
cells. Here we examine in detail the properties of BK channels in RIN
and HIT cells using inside-out patches and whole cell recordings. BK
channels in RIN cells exhibit rapid inactivation that results in an
anomalous steady-state Ca2+ dependence of activation. In
contrast, BK channels in HIT cells exhibit the more usual
noninactivating behavior. When BK inactivation is taken into account,
the Ca2+ and voltage dependence of activation of BK
channels in RIN and HIT cells is essentially indistinguishable. The
properties of BK channel inactivation in RIN cells are similar to those
of inactivating BK channels (termed BKi channels)
previously identified in rat chromaffin cells. Inactivation involves
multiple, trypsin-sensitive cytosolic domains and exhibits a dependence
on Ca2+ and voltage that appears to arise from coupling to
channel activation. In addition, the rates of inactivation onset and
recovery are similar to that of BKi channels in chromaffin
cells. The charybdotoxin (CTX) sensitivity of BKi currents
is somewhat less than that of the noninactivating BK variant. Action
potential voltage-clamp waveforms indicate that BK current is activated
only weakly by Ca2+ influx in RIN cells but more strongly
activated in HIT cells even when Ca2+ current magnitude is
comparable. Concentrations of CTX sufficient to block BKi
current in RIN cells have no effect on action potential activity
initiated by glucose or DC injection. Despite its abundant expression
in RIN cells, BKi current appears to play little role in
action potential activity initiated by glucose or DC injection in RIN
cells, but BK current may play an important role in action potential
repolarization in HIT cells.
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