Abstract
ABSTRACT Cooling caused axonal depolarization in desheathed and urea-treated connectives, but induced hyperpolarizing responses (measured with microelectrodes and with the sucrose-gap) in intact preparations. Hyperpolarizing responses were also recorded with extracellularly-located microelectrodes in intact connectives. Strophanthidin (0·2 mm/1) caused axonal depolarization in desheathed preparations, ethacrynic acid being without appreciable effect. Ethacrynic acid (0·2 mm/1) induced apparent hyperpolarizations in intact connectives and abolished or reduced the effects of cooling. It is concluded that the axonal sodium pump is pharmacologically separable from that associated with the perineurial and/or the glial membranes: the former being inhibited by cardiac glycosides, the latter by ethacrynic acid. The results are discussed in relation to extra-axonal sodium regulation and the possible involvement of an electrogenic sodium pump associated with the perineurial or glial membranes.
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