ORIGIN OF POSTDEPOLARIZATION HYPERPOLARIZATIONS IN A GREASE-GAP RECORDING PREPARATION

In grease-gap recording preparations, depolarizing responses evoked by agonists are often followed by a hyperpolarization (post-depolarizati on hyperpolarization). We have investigated the origin of these post-d epolarization hyperpolarizations in the rat CA1-subiculum slice. They were evoked by L-glutamate, N-methyl-d-aspartate or ha-amino-3-hydroxy -5-methyl-isoxazole-4-propionate in approximately 80 % of the slices t ested. The post-depolarization hyperpolarizations evoked by perfusion of N-methyl-d-aspartate through the CA1 compartment of the chamber, pe rsisted when N-methyl-d-aspartate receptors in the subicular compartme nt were blocked with D-2-amino-5-phosphonopentanoate. Carbachol only b locked the post-depolarization hyperpolarizations evoked by ha-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 Ca2+-free medium and by admi nistration of ouabain, and showed a marked sensitivity to temperature. It is concluded that the post-depolarization hyperpolarizations obser ved in this preparation are not a consequence of diffusion of the agon ist through the slice. The evidence is, however, consistent with them being generated by activation of the electrogenic Na+-K+ pump, althoug h we cannot exclude an additional contribution from Ca2+ - or voltage- dependent K+ currents.