Temperature effects on resting potential and spike parameters of cat motoneurons.

Abstract

During intracellular recording from cat spinal motoneurons, the lumbo-sacral cord was subjected to rapid local temperature changes. Cooling to 30° C causes a decrease in the resting membrane potential (RMP), a transient increase in spike overshoot, and increases in the input resistance and the durations of both the action potential and the hyperpolarizing after-potential (HAP). Warming causes these membrane parameters to change in the opposite direction and can result in a failure of antidromic activation. The RMP changes are dependent upon the RMP at normal temperature, being negligible in cells having an initial RMP greater than 70 mV. The Q10-values of the three peaks of the differentiated spike are relatively high and nearly identical to the Q10-values of the corresponding rate constants for sodium activation and inactivation and potassium activation measured by Frankenhaeuser and Moore in toad nerve fibers, i.e. 1.71, 2.35 and 3.12, respectively. Delayed sodium inactivation and potassium activation explain the increase in spike overshoot observed during cooling, and the high Q10 of potassium activation is nearly identical to the Q10 of the time to peak of the HAP (3.12 vs. 2.97). The decrease in RMP during cooling is attributed to a decrease in the PK∶PNa ratio rather than to a blockage of an electrogenic sodium pump; the differences in RMP temperature sensitivities between cells with high and low initial RMP's might be due to a higher resting PK (anomalous rectification) at higher RMP. We conclude that the electrogenic pump does not normally contribute significantly to the RMP of cat motoneurons.