AJP - Cell Physiology, Vol 262, Issue 5 C1335-C1340, Copyright © 1992 by American Physiological Society
Characterization of a delayed rectifier potassium current in chicken growth plate chondrocytes
K. B. Walsh, S. D. Cannon and R. E. Wuthier
Department of Pharmacology, University of South Carolina School of Medicine, Columbia 29208.
With the use of the whole cell arrangement of the patch-clamp technique, an
outward-directed time-dependent potassium current was identified in
cultured chicken growth plate chondrocytes. This delayed rectifier
potassium current (IK) activated with a sigmoidal time course during
voltage steps to potentials positive to -40 mV. The half-maximal voltage
required for current activation was determined to be -8 mV. The reversal
potential (Erev) for IK, measured using deactivating tail currents, was -72
mV in the presence of 140 mM internal and 5 mM external [K+] solutions.
Changes in external [K+] caused Erev to shift in a manner expected for a
potassium-selective channel. In addition, increasing external [K+] from 5
to 50 mM caused the slope conductance of the tail currents to increase
twofold. The chondrocyte IK was inhibited by the potassium-channel blocker
4-aminopyridine (4-AP) at concentrations of 0.5-4 mM and by the scorpion
venom toxin charybdotoxin (CTX; 10 nM) but was unaffected by 10 mM
tetraethylammonium (TEA). Addition of 20 microM ZnCl2 reduced IK in a
voltage-dependent manner with the greatest inhibition found to occur at
potentials near the threshold for current activation. Reduction of IK by
ZnCl2 was accompanied by a slowing in the kinetics of IK activation. On the
basis of the gating and pharmacological properties of this current, it is
suggested that the chondrocyte channel belongs to a superfamily of K+
channels found in bone and immune system cells. The chondrocyte K+ channel
may contribute to the unusually high [K+] found in the extracellular fluid
of growth plate cartilage.
