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- W4309651431 abstract "Abstract Epileptic seizures are widely regarded to occur as a result of the excitation-inhibition imbalance from a neuro-centric view. Although astrocyte-neuron interactions are increasingly recognized in seizure, elementary questions about the causal role of astrocytes in seizure remain unanswered. Here we show that optogenetic activation of channelrhodopsin-2-expressing astrocytes effectively attenuates neocortical seizures in rodent models. This anti-seizure effect is independent from classical calcium signaling, and instead related to astrocytic Na + -K + -ATPase-mediated buffering K + , which activity-dependently inhibits firing in highly active pyramidal neurons during seizure. Compared with inhibition of pyramidal neurons, astrocyte stimulation exhibits anti-seizure effects with several advantages, including a wider therapeutic window, large-space efficacy, and minimal side effects. Finally, optogenetic-driven astrocytic Na + -K + -ATPase shows promising therapeutic effects in a chronic focal cortical dysplasia epilepsy model. Together, we uncover a promising anti-seizure strategy with optogenetic control of astrocytic Na + -K + -ATPase activity, providing alternative ideas and a potential target for the treatment of intractable epilepsy." @default.
- W4309651431 created "2022-11-29" @default.
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- W4309651431 date "2022-11-21" @default.
- W4309651431 modified "2023-10-03" @default.
- W4309651431 title "Activated astrocytes attenuate neocortical seizures in rodent models through driving Na+-K+-ATPase" @default.
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- W4309651431 doi "https://doi.org/10.1038/s41467-022-34662-2" @default.
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- W4309651431 hasPublicationYear "2022" @default.
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