The electrophysiological properties of voltage
dependent potassium channels from freshly
dissociated rat articular chondrocytes were studied.
The resting membrane potential (-42.7±2.0 mV) was
significantly depolarized by increasing concentrations
of external potassium. No change was observed when
external chloride concentration was varied. Addition
of TEA, 4AP, α-Dendrotoxin and charybdotoxin
depolarized resting membrane potential. Whole cell
patch clamp studies revealed the presence of
outwardly rectifying currents whose kinetic and
pharmacological properties suggest the expression
of voltage dependent potassium channels. Two kinds
of currents were observed under the same
experimental conditions. The first one, most frequently
observed (80%), starts activating near -50 mV, with
V1/2=-18 mV, Gmax=0.30 pS/pF. The second kind was
observed in only 10% of cases; It activates near -40
mV, with1/2=+28.35 mV, Gmax=0.28 pS/pF pA/pF and
does not inactivates. Inactivating currents were
significantly inhibited by TEA (IC50=1.45 mM), 4AP
(IC50=0.64 mM), CTX (IC50≈10 nM), α-Dendrotoxin
(IC50 < 100 nM) and Margatoxin (IC50=28.5 nM). These
results show that rat chondrocytes express voltage
dependent potassium currents and suggest a role of
voltage-dependent potassium channels in regulating
membrane potential of rat chondrocytes.