Articular cartilage creates a durable, elastic and virtually frictionless interface between jointed bones. A high fixed charge density in cartilage osmotically binds interstitial fluid which distends and stiffens the tissue. Damage or disease can alter the fluid content or the charge density of cartilage which then compromises its mechanical performance. This can lead to further cartilage damage and joint deterioration.

Cartilage health is maintained by chondrocytes which reside in lacunae within the cartilage and are responsible for the synthesis and maintenance of the surrounding tissue. Matrix synthesis rates are known to be altered by mechanical loads within the tissue. This mecbanotransduction allows chondrocytes to maintain the homeostasis of the extracellular matrix material. Mechanotransduction mechanisms for chondrocytes are poorly understood, but electrophysiological changes are a likely candidate.

This study measured the electrophysiology of chondrocytes under different mechanical and osmotic loading conditions. Patch clamp experiments recorded membrane currents and voltages from freshly isolated canine chondrocytes. Currents were also recorded from individual ion channels using single channel recording methods.

Chondrocytes were found to have a resting potential of —38 mV, and membrane currents had a pronounced voltage sensitivity. The peak membrane current of resting, unloaded chondrocytes was found to average 156 pA, which is small compared to other cell types. Channel blocking experiments and equilibrium potential considerations established that the membrane current is dominated by K⁺. Direct mechanical loading of the cell by intracellular suction or pressure, or by compressing the cell with a blunt pipette did not alter the membrane current. However, stretching the cell by hypotonic shock resulted in a 40-fold current increase 5 minutes after the hypotonic shock. The large swelling current is sensitive to K⁺ channel blockers and stretch-activated channel blockers.

The first mathematical model of chondrocyte electrophysiology was developed. The model was initially compared to the established Hodgkin-Huxley model for neuron electrophysiology;​ then applied to chondrocyte data from this study and from literature. The model demonstrated that the swelling current is effective at regulating chondrocyte volume under hypotonic shock.