Origin of post-depolarization hyperpolarizations in a grease-gap recording preparation

In grease-gap recording preparations, depolarizing responses evoked by agonists are often followed by a hyperpolarization (post-depolarization hyperpolarization). We have investigated the origin of these post-depolarization hyperpolarizations in the rat CA1-subiculum slice. They were evoked by L-glutamate, N-methyl-d-aspartate or alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate in approximately 80% of the slices tested. The post-depolarization hyperpolarizations evoked by perfusion of N-methyl-d-aspartate through the CA1 compartment of the chamber, persisted when N-methyl-d-aspartate receptors in the subicular compartment were blocked with D-2-amino-5-phosphonopentanoate. Carbachol only blocked the post-depolarization hyperpolarizations evoked by alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate at concentrations which also blocked the depolarization. The post-depolarization hyperpolarization was selectively blocked by perfusion with Ca(2+)-free medium and by administration of ouabain, and showed a marked sensitivity to temperature. It is concluded that the post-depolarization hyperpolarizations observed in this preparation are not a consequence of diffusion of the agonist through the slice. The evidence is, however, consistent with them being generated by activation of the electrogenic Na(+)-K+ pump, although we cannot exclude an additional contribution from Ca(2+)- or voltage-dependent K+ currents.