Astrocyte switch to the hyperactive mode.

Autor: Araki S; Super-network Brain Physiology, Graduate School of Medicine, Tohoku University, Sendai, Japan., Onishi I; Super-network Brain Physiology, Graduate School of Medicine, Tohoku University, Sendai, Japan., Ikoma Y; Super-network Brain Physiology, Graduate School of Life Sciences, Tohoku University, Sendai, Japan., Matsui K; Super-network Brain Physiology, Graduate School of Medicine, Tohoku University, Sendai, Japan.; Super-network Brain Physiology, Graduate School of Life Sciences, Tohoku University, Sendai, Japan.
Jazyk: angličtina
Zdroj: Glia [Glia] 2024 Aug; Vol. 72 (8), pp. 1418-1434. Date of Electronic Publication: 2024 Apr 09.
DOI: 10.1002/glia.24537
Abstrakt: Increasing pieces of evidence have suggested that astrocyte function has a strong influence on neuronal activity and plasticity, both in physiological and pathophysiological situations. In epilepsy, astrocytes have been shown to respond to epileptic neuronal seizures; however, whether they can act as a trigger for seizures has not been determined. Here, using the copper implantation method, spontaneous neuronal hyperactivity episodes were reliably induced during the week following implantation. With near 24-h continuous recording for over 1 week of the local field potential with in vivo electrophysiology and astrocyte cytosolic Ca 2+ with the fiber photometry method, spontaneous occurrences of seizure episodes were captured. Approximately 1 day after the implantation, isolated aberrant astrocyte Ca 2+ events were often observed before they were accompanied by neuronal hyperactivity, suggesting the role of astrocytes in epileptogenesis. Within a single developed episode, astrocyte Ca 2+ increase preceded the neuronal hyperactivity by ~20 s, suggesting that actions originating from astrocytes could be the trigger for the occurrence of epileptic seizures. Astrocyte-specific stimulation by channelrhodopsin-2 or deep-brain direct current stimulation was capable of inducing neuronal hyperactivity. Injection of an astrocyte-specific metabolic inhibitor, fluorocitrate, was able to significantly reduce the magnitude of spontaneously occurring neuronal hyperactivity. These results suggest that astrocytes have a role in triggering individual seizures and the reciprocal astrocyte-neuron interactions likely amplify and exacerbate seizures. Therefore, future epilepsy treatment could be targeted at astrocytes to achieve epilepsy control.
(© 2024 The Authors. GLIA published by Wiley Periodicals LLC.)
Databáze: MEDLINE
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