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Ca 2+  signaling in glial cells is primarily triggered by metabotropic pathways and the subsequent Ca 2+  release from internal Ca 2+  stores. However, there is upcoming evidence that various ion channels might also initiate Ca 2+  rises in glial cells by Ca 2+  influx. We investigated AMPA receptor-mediated inward currents and Ca 2+  transients in olfactory ensheathing cells (OECs), a specialized glial cell population in the olfactory bulb (OB), using whole-cell voltage-clamp recordings and confocal Ca 2+  imaging. By immunohistochemistry we showed immunoreactivity to the AMPA receptor subunits GluA1, GluA2 and GluA4 in OECs, suggesting the presence of AMPA receptors in OECs. Kainate-induced inward currents were mediated exclusively by AMPA receptors, as they were sensitive to the specific AMPA receptor antagonist, GYKI53655. Moreover, kainate-induced inward currents were reduced by the selective Ca 2+ -permeable AMPA receptor inhibitor, NASPM, suggesting the presence of functional Ca 2+ -permeable AMPA receptors in OECs. Additionally, kainate application evoked Ca 2+  transients in OECs which were abolished in the absence of extracellular Ca 2+ , indicating that Ca 2+  influx via Ca 2+ -permeable AMPA receptors contribute to kainate-induced Ca 2+  transients. However, kainate-induced Ca 2+  transients were partly reduced upon Ca 2+  store depletion, leading to the conclusion that Ca 2+  influx via AMPA receptor channels is essential to trigger Ca 2+  transients in OECs, whereas Ca 2+  release from internal stores contributes in part to the kainate-evoked Ca 2+  response. Endogenous glutamate release by OSN axons initiated Ca 2+  transients in OECs, equally mediated by metabotropic receptors (glutamatergic and purinergic) and AMPA receptors, suggesting a prominent role for AMPA receptor mediated Ca 2+  signaling in axon-OEC communication.

AMPA Receptor-Mediated Ca2+ Transients in Mouse Olfactory Ensheathing Cells