Changes in extracellular potassium and calcium in rat cerebellar cortex related to local inhibition of the sodium pump.

Extracellular K+, Ca2+, and Na+ ([K+]e, [Ca2+]e, [Na+]e) were recorded with ion selective microelectrodes in the cerebellar cortex of urethane-anesthetized rats. Superfusion of the cerebellum with artificial cerebrospinal fluid containing K-strophanthidin (10(-6)-10(-4) mol/l) or other cardioactive steroids, known to be inhibitors of the sodium/potassium pump, had the following effects: elevation of resting [K+]e, reduction of poststimulus K+-undershoots, decrease of resting [Ca2+]e and [Na+]e. For instance, at 3 X 10(-5) mol/l K-strophanthidin within the superfusion solution (the unknown intracerebellar concentration being certainly much smaller), [K+]e was elevated up to 130% and [Ca2+]e reduced to 70% of their resting values. Iontophoretic K+-pulses were enhanced in amplitude at the same time. Control experiments with iontophoretic TMA application demonstrated that the glycoside effects were not due (or in higher concentrations only partly due) to shrinkage of the extracellular fluid volume. When tetrodotoxin (10(-7) mol/l) or Mn2+ (1-3 mmol/l) were additionally superfused, K-strophanthidin effects were qualitatively similar, though quantitatively smaller. This indicates that part of the effects were indirect via neuronal activity evoked by the blockade of the sodium pump. The experiments show that reduction of sodium pump activity in cerebellar cortex has rapid and serious consequences on the distribution of potassium and calcium in the extracellular space, resulting in an alteration of neuronal circuit excitability.