REDUCTION OF K-TERM DEPRESSION MAINTENANCE AND CAUSES EPILEPTIFORM ACTIVITY( UPTAKE IN GLIA PREVENTS LONG)

Extracellular cesium causes synchronous, interictal-like bursting and prevents maintenance of long-term depression (LTD) in the CAI hippocam pal region. We have investigated the cellular mechanisms underlying ce sium actions. Whole-cell recordings showed that brief (2 min) bath exp osures to cesium caused pyramidal cell hyperpolarization associated wi th decreased membrane conductance attributable to blockade of an inwar d h-type current. After prolonged (>2 min) exposures, a late depolariz ing response was observed; this effect was not associated with changes in cell membrane conductance. Recordings from interneurons revealed t hat I-h is expressed in a subpopulation of cells and that cesium effec ts on interneurons expressing I-h are comparable to those observed in pyramidal cells. Consistent with this effect, cesium decreased the ear ly component of the IPSP recorded in pyramidal cells. Interneurons lac king I-h were not affected by cesium but developed a depolarizing resp onse when drug applications were paired to orthodromic stimulation. We concluded that cesium actions on LTD and cesium-induced epileptiform activity were not attributable exclusively to its direct effects on ne urons. Recordings from hippocampal slice astrocytes revealed that cesi um interfered with glial electrical responses during LTD induction. Ce sium blocked glial inwardly rectifying potassium channels and increase d the amplitude and duration of stimulation-evoked [K+](out) increases . Thus, the effects of cesium on CAI synchronization and synaptic plas ticity appear to be mediated predominantly by blockade of glial voltag e-dependent potassium uptake.