KAINATE ACTIVATES CA2-PERMEABLE GLUTAMATE RECEPTORS AND BLOCKS VOLTAGE-GATED K+ CURRENTS IN GLIAL-CELLS OF MOUSE HIPPOCAMPAL SLICES()

Glial cells in the CA1 stratum radiatum of the hippocampus of 9- to 12 -day-old mice show intrinsic responses to glutamate due to the activat ion of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA)/ka inate receptors. In the present study we have focused on a subpopulati on of the hippocampal glial cells, the ''complex'' cells, characterize d by voltage-gated Na+ and K+ channels. Activation of glutamate recept ors in these cells led to two types of responses, the activation of a cationic conductance, and a longer-lasting blockade of voltage-gated K + channels. In particular, the transient (inactivating) component of t he outwardly rectifying K+ current was diminished by kainate. Concomit antly, as described in Bergmann glial cells, kainate also elevated cyt osolic Ca2+. This increase was due to an influx via the glutamate rece ptor itself. In contrast to Bergmann glial cells, the cytosolic Ca2+ i ncrease was not a link to the K+ channel blockade, since the blockade occurred in the absence of the Ca2+ signal and, vice versa, an increas e in cytosolic Ca2+ induced by ionomycin did not block the transient K + current. We conclude that glutamate receptor activation leads to com plex and variable changes in different types of glial cells; the funct ional importance of these changes is as yet unresolved.