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The systemic exposure of adult rats to TCE (1000 mg/Kg/day/5 days a week/2 and 6 weeks, oral gavage) inhibits mitochondrial complex I enzyme activity, increases oxidative stress markers, activates the microglia, induces nigral -syn accumulation and a significant loss of dopaminergic neurons on the SNpc in a dose-dependent manner, as well as defects in the rotarod behavior test (Liu et al., 2010)

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Metabolism of GABA along the pathway suggested in Figure 7 would eliminate a need for uptake of exogenous aspartate and its conversion to malate in astrocytes in an aspartate-dependent pathway model for GABA formation suggested by LaNoue et al