Recent Ca2+ imaging studies in cell culture and in sial have shown that Ca2
+ elevations in astrocytes stimulate glutamate release and increase neurona
l Ca2+ levels, and that this astrocyte-neuron signaling can be stimulated b
y prostaglandin E-2 (PGE(2)). We investigated the electrophysiological cons
equences of the PGE(2)-mediated astrocyte-neuron signaling using whole-cell
recordings on cultured rat hippocampal cells. Focal application of PGE, to
astrocytes evoked a Ca2+ elevation in the stimulated cell by mobilizing in
ternal Ca2+ stores, which further propagated as a Ca2+ wave to neighboring
astrocytes. Whole-cell recordings from neurons revealed that PGE(2) evoked
a slow inward current in neurons adjacent to astrocytes, This neuronal resp
onse required the presence of an astrocyte Ca2+ wave and was mediated throu
gh both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors. Taken
together with previous studies, these data demonstrate that PGE(2)-evoked
Ca2+ elevations in astrocyte cause the release of glutamate which activates
neuronal ionotropic receptors. (C) 1999 John Wiley & Sons, Inc.