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- W3211323914 endingPage "e1009871" @default.
- W3211323914 startingPage "e1009871" @default.
- W3211323914 abstract "Kohlschütter-Tönz syndrome (KTS) manifests as neurological dysfunctions, including early-onset seizures. Mutations in the citrate transporter SLC13A5 are associated with KTS, yet their underlying mechanisms remain elusive. Here, we report that a Drosophila SLC13A5 homolog, I'm not dead yet (Indy), constitutes a neurometabolic pathway that suppresses seizure. Loss of Indy function in glutamatergic neurons caused bang-induced seizure-like behaviors. In fact, glutamate biosynthesis from the citric acid cycle was limiting in Indy mutants for seizure-suppressing glutamate transmission. Oral administration of the rate-limiting α-ketoglutarate in the metabolic pathway rescued low glutamate levels in Indy mutants and ameliorated their seizure-like behaviors. This metabolic control of the seizure susceptibility was mapped to a pair of glutamatergic neurons, reversible by optogenetic controls of their activity, and further relayed onto fan-shaped body neurons via the ionotropic glutamate receptors. Accordingly, our findings reveal a micro-circuit that links neural metabolism to seizure, providing important clues to KTS-associated neurodevelopmental deficits." @default.
- W3211323914 created "2021-11-08" @default.
- W3211323914 creator A5000079450 @default.
- W3211323914 creator A5038871139 @default.
- W3211323914 creator A5042458320 @default.
- W3211323914 creator A5066995407 @default.
- W3211323914 date "2021-10-29" @default.
- W3211323914 modified "2023-10-14" @default.
- W3211323914 title "Metabolic flux from the Krebs cycle to glutamate transmission tunes a neural brake on seizure onset" @default.
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