THE ELECTROGENIC SODIUM PUMP AND CONDUCTANCE CHANGES IN THE POST-TETANIC HYPERPOLARIZATION OF CRAYFISH MEDIAN GIANT AXONS

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Abstract
The post-tetanic hyperpolarization (PTH) mechanism was investigated using the intracellular recording technique. The median giant axon of a crayfish [Procambarus clarkii] 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. An increase in K+ conductance contributed 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 [dinitrophenol], or by cooling. These procedures shifted the reversal potential in the depolarizing direction. With K+ absent, PTH was partly due to the activity of an electrogenic Na pump. With lowering of external Na+ concentration, PTH became larger and the reversal potential moved in the hyperpolarizing direction. Na+ conductance increased when PTH was elicited, probably as the amount of Na+ entering per impulse and the activation of the Na pump reduced by reducing Na+ concentration in the external medium. PTH in the median giant axons of crayfish was produced by at least 2 mechanisms: an increase in activity of the electrogenic Na pump, and an increase of membrane conductance to K+ and Na+.