Calcium-sensitive recovery of extracellular potassium and synaptic transmission in rat hippocampal slices exposed to brief anoxia

Abstract

We examined the possibility that Ca 2+-sensitive inhibition of synaptic transmission following anoxia involves compromise of ion transport activity. Rat hippocampal slices were superfused with artificial cerebrospinal fluids containing different concentrations of CaCl 2, and subjected to short anoxia. Durations of anoxia were sufficient to provoke anoxic depolarization, indicated by a sudden rise in extracellular K + (K + o). Following anoxia, apparent K + transport was assessed by measuring the magnitude of subnormal K + o (the K + o undershoot) in hippocampal region CA 1. Recovery of synaptic transmission 1 h after anoxia was determined by evaluation of the magnitudes of the orthodromically stimulated population spike recorded from CA 1 pyramidal cells. K + o undershoots and recovery of synaptic transmission decreased as CaCl 2 or the duration of anoxic depolarization increased. These data suggest: (1) that increased artificial cerebrospinal fluid CaCl 2 compromised K + reaccumulation after anoxia; and (2) that ion transport dysfunction may inhibit recovery of synaptic transmission.