Ca(2+)-permeable AMPA receptors in mouse olfactory bulb astrocytes

Ca(2+) signaling in astrocytes is considered to be mainly mediated by metabotropic receptors linked to intracellular Ca(2+) release. However, recent studies demonstrate a significant contribution of Ca(2+) influx to spontaneous and evoked Ca(2+) signaling in astrocytes, suggesting that Ca(2+) influx might account for astrocytic Ca(2+) signaling to a greater extent than previously thought. Here, we investigated AMPA-evoked Ca(2+) influx into olfactory bulb astrocytes in mouse brain slices using Fluo-4 and GCaMP6s, respectively. Bath application of AMPA evoked Ca(2+) transients in periglomerular astrocytes that persisted after neuronal transmitter release was inhibited by tetrodotoxin and bafilomycin A1. Withdrawal of external Ca(2+) suppressed AMPA-evoked Ca(2+) transients, whereas depletion of Ca(2+) stores had no effect. Both Ca(2+) transients and inward currents induced by AMPA receptor activation were partly reduced by Naspm, a blocker of Ca(2+)-permeable AMPA receptors lacking the GluA2 subunit. Antibody staining revealed a strong expression of GluA1 and GluA4 and a weak expression of GluA2 in periglomerular astrocytes. Our results indicate that Naspm-sensitive, Ca(2+)-permeable AMPA receptors contribute to Ca(2+) signaling in periglomerular astrocytes in the olfactory bulb.