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Journal Article

Ca2+ signals in astrocytes facilitate spread of epileptiform activity

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Sprengel,  Rolf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Heuser, K., Nome, C. G., Pettersen, K. H., Åbjørsbråten, K. S., Jensen, V., Tang, W., et al. (2018). Ca2+ signals in astrocytes facilitate spread of epileptiform activity. Cerebral Cortex, 28(11), 4036-4048. doi:10.1093/cercor/bhy196.


Cite as: https://hdl.handle.net/21.11116/0000-0002-E3C4-0
Abstract
Epileptic seizures are associated with increased astrocytic Ca2+ signaling, but the fine spatiotemporal kinetics of the ictal astrocyte-neuron interplay remains elusive. By using 2-photon imaging of awake head-fixed mice with chronic hippocampal windows we demonstrate that astrocytic Ca2+ signals precede neuronal Ca2+ elevations during the initial bout of kainate-induced seizures. On average, astrocytic Ca2+ elevations preceded neuronal activity in CA1 by about 8 s. In subsequent bouts of epileptic seizures, astrocytes and neurons were activated simultaneously. The initial astrocytic Ca2+ elevation was abolished in mice lacking the type 2 inositol-1,4,5-trisphosphate-receptor (Itpr2-/-). Furthermore, we found that Itpr2-/- mice exhibited 60% less epileptiform activity compared with wild-type mice when assessed by telemetric EEG monitoring. In both genotypes we also demonstrate that spreading depression waves may play a part in seizure termination. Our findings imply a role for astrocytic Ca2+ signals in ictogenesis.