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• W2120083721 abstract "Abstract In this study we tested the hypothesis that the 65‐kDa isoform of glutamate decarboxylase (GAD 65 ) mediates activity‐dependent GABA synthesis as invoked by seizures in anesthetized rats. GABA synthesis was measured following acute GABA‐transaminase inhibition by gabaculine using spatially localized 1 H NMR spectroscopy before and after bicuculline‐induced seizures. Experiments were conducted with animals pre‐treated with vigabatrin 24 h earlier in order to reduce GAD 67 protein and also with non‐treated controls. GAD isoform content was quantified by immunoblotting. GABA was higher in vigabatrin‐treated rats compared to non‐treated controls. In vigabatrin‐treated animals, GABA synthesis was 28% lower compared to controls [ p < 0.05; vigabatrin‐treated, 0.043 ± 0.011 µmol/(g min); non‐treated, 0.060 ± 0.014 µmol/(g min)] and GAD 67 was 60% lower. No difference between groups was observed for GAD 65 . Seizures increased GABA synthesis in both control [174%; control, 0.060 ± 0.014 µmol/(g min) vs. seizures, 0.105 ± 0.043 µmol/(g min)] and vigabatrin‐treated rats [214%; control, 0.043 ± 0.011 µmol/(g min); seizures, 0.092 ± 0.018 µmol/(g min)]. GAD 67 could account for at least half of basal GABA synthesis but only 20% of the two‐fold increase observed in vigabatrin‐treated rats during seizures. The seizure‐induced activation of GAD 65 in control cortex occurs concomitantly with a 2.3‐fold increase in inorganic phosphate, known to be a potent activator of apoGAD 65 in vitro . Our results are consistent with a major role for GAD 65 in activity‐dependent GABA synthesis." @default.
• W2120083721 created "2016-06-24" @default.
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• W2120083721 date "2006-03-15" @default.
• W2120083721 modified "2023-10-16" @default.
• W2120083721 title "Evidence that GAD₆₅mediates increased GABA synthesis during intense neuronal activity<i>in vivo</i>" @default.
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• W2120083721 doi "https://doi.org/10.1111/j.1471-4159.2006.03741.x" @default.
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