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Glucose trafficking through coupled astrocytes is necessary for hyperactivity, while extracellular glucose deprivation causes loss of synaptic hyperactivity that can be rescued when astrocytes are filled with glucose or lactate, showing the importance of metabolism in epilepsy formation

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Interestingly, GSAAT(WT), GSAAT(C138S) and GSAAT(C396S) lines were still markedly redox responsive, and exhibited up to 20% higher enzyme activity when supplied with DTT relative to the UT control conditions, while the two gsa2 lines expressing GSAAT(C168S) and GSAAT(C190S) resulted only in 9% and 2% increased GSAAT activity upon addition of DTT to the extracts ( Supplementary Figure 3E )