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Impairment of GABAergic system contributes to epileptogenesis in glutaric acidemia type I

Glutaric acidemia type I (GA‐I) is an inherited neurometabolic disorder caused by deficiency of glutaryl‐CoA dehydrogenase (GCDH) and characterized by increased levels of glutaric, 3‐OH‐glutaric, and glutaconic acids in the brain parenchyma. The increment of these organic acids inhibits glutamate decarboxylase (GAD) and consequently lowers the γ‐aminobutyric acid (GABA) synthesis. Untreated patients exhibit severe neurologic deficits during development, including epilepsy, especially following an acute encephalopathy outbreak. In this work, we evaluated the role of the GABAergic system on epileptogenesis in GA‐I using the Gcdh−/− mice exposed to a high lysine diet (Gcdh−/−‐Lys).