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Highlights d Reactive astrocytes in SNpc produce excessive GABA via MAO-B in animal models of PD d Aberrant tonic inhibition causes reduced DA production in neurons and motor deficits d Dormant neurons are rescued by MAO-B inhibition or optogenetic neuronal activation

Highlights d Capsular infarct induces neuronal atrophy and reactive astrogliosis in motor cortex d Tonic GABA from reactive astrocytes suppresses neuronal glucose metabolism d Inhibition of MAO-B, the GABA-synthesizing enzyme, restores glucose metabolism d Combined therapy of MAO-B inhibitor and rehabilitation causes functional recovery