Expression of Voltage Dependent Potassium Currents in Freshly Dissociated Rat Articular Chondrocytes

Abstract

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 V_1/2=-18 mV, G_max=0.30 pS/pF. The second kind was observed in only 10% of cases; It activates near -40 mV, with_1/2=+28.35 mV, G_max=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.

Calcium Input Potentiates the Transforming Growth Factor (TGF)-β1-dependent Signaling to Promote the Export of Inorganic Pyrophosphate by Articular Chondrocyte

“…TGF-␤1 was also shown to modify the cell membrane voltage by modulating K ϩ currents in microglia cells (41). Interestingly, rat articular chondrocytes express such K ϩ channels (42), suggesting that electrophysiological changes may have contributed to the observed IP 3 -independent mechanism. Altogether, these findings support the hypothesis of a quick TGF-␤1-mediated modification of the K ϩ currents, resulting in the opening of L-and T-VOCs, and secondary calcium influx into chondrocytes.…”

Accelerated Ca2+ entry by membrane hyperpolarization due to Ca2+-activated K+ channel activation in response to histamine in chondrocytes

“…Since the functional expression of voltage-gated K ϩ (Kv) channels in chondrocytes has been reported (18,20,24,40,41), the possibility that Kv channel activation by histamine contributes to the membrane hyperpolarization cannot be excluded completely. This may be, however, unlikely based on the amplitude of remaining hyperpolarization induced by histamine in the presence of BK, IK, and SK channel blockers.…”

“…Electrophysiological studies have revealed the presence of voltage-gated Na ϩ channels (30), Cl Ϫ channels (30,35), and H ϩ channels (27). In addition, several types of K ϩ channels-voltage-gated K ϩ channels (18,20,24,40,41), large-conductance Ca 2ϩ -activated K ϩ (BK) channels (7), and stretch-activated K ϩ channels (15,19)-have been identified. Pharmacological studies suggest the presence of an even wider diversity of channel expression in chondrocytes.…”

Voltage-gated K+currents in mouse articular chondrocytes regulate membrane potential

“…A number of these could contribute to membrane potential. For example, electrophysiological studies in isolated chondrocytes have directly identified voltage-gated, [11][12][13][14] Ca 2+ -activated, 15 ATP-sensitive 16 and stretch-activated 17 K + channels. Non-specific cation channels, 18 voltage-activated 19 and swelling-activated 20,21 Cl -and voltagegated H + , 22 channels have also been recorded in isolated chondrocytes.…”

“…Currents over the potential range from -110 mV to about -60 mV were circumstances. For example, previous in vitro electrophysiological studies have shown that voltage-gated K + channels contribute to membrane potential of 'resting' rat 14 and dog 12 articular chondrocytes. Activation of 'small conductance' Ca 2+ -activated K + channels was suggested to underlie the apamin-sensitive membrane hyperpolarization of human articular chondrocytes that followed repetitive mechanical stimulation.…”