Activation of electrogenic sodium pump in hippocampal CA1 neurons following glutamate-induced depolarization.

Intracellular recordings were obtained from guinea pig hippocampal CA1 pyramidal neurons maintained in vitro. Focal applications of glutamate produced depolarizations followed by prolonged hyperpolarizations. The mechanisms underlying this postglutamate hyperpolarization (PGH) were investigated. PGH did not reverse polarity with hyperpolarization to potentials at or near the presumed K+ equilibrium potential. A transient increase in conductance was associated with the PGH; control values returned well before the termination of PGH. Application of Mn2+, an antagonist of voltage-dependent calcium conductance, blocked synaptic transmission and the afterhyperpolarization (AHP) that follows a directly evoked train of action potentials but did not diminish the PGH or the transient conductance increase. Intracellular application of the calcium chelator ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid blocked AHP but did not affect PGH. Reductions in temperature from 37 to 27-32 degrees C reduced the amplitude of PGH and prolonged its duration but increased the amplitude and duration of AHP. The transient conductance increase associated with PGH was unaffected. Application of strophanthidin, a specific antagonist of Na+-K+-ATPase, reversibly blocked PGH and led to large increases in the amplitude and duration of the AHP. It is concluded that PGH is produced by activation of the electrogenic sodium pump by glutamate-induced excitation. As such, PGH is a useful physiological assay of electrogenic sodium transport. In addition, maintenance of the Na+ gradient by the sodium pump is important for the buffering of Ca2+ influx.