The electrogenic sodium pump and conductance changes in the post-tetanic hyperpolarization of crayfish median giant axons.

Abstract

The mechanism of post-tetanic hyperpolarization (PTH) occurrence was investigated using the intracellar recording technique. The median giant axon of a crayfish abdominal nerve cord was repetitively stimulated to elicit PTH. When the membrane potential was hyperpolarized by intracellularly applied currents, PTH reversed its sign. K+ removal from the external medium increased the size of PTH and shifted its reversal potential in the hyperpolarizing direction. This results shows that an increase in K+ conductance contributes to the formation of PTH. In a K+-free medium, the size of PTH was reduced by replacement of Na+ with Li+ in the external medium, by application of ouabain or DNP, or by cooling. These procedures shifted the reversal potential in the depolarizing direction. These findings are interpreted as showing that, with K+ absent, PTH is partly due to the activity of electrogenic Na pump. With lowering of external Na+ concentration, PTH became larger and the reversal potential moved in the hyperpolarizing direction. The experiment suggests that Na+ conductance is also increased when PTH is elicited because one expects the amount of Na+ entering per impulse and the activation of the Na pump to be reduced by reducing Na+ concentration in the external medium. It is concluded that PTH in the median giant axons of crayfish is produced by at least two mechanisms. One is an increase in activity of the electrogenic Na pump, and the other is an increase of membrane conductance to K+ and Na+.