GLYAT and Parkinson disease: The DA release deficit in a model of familial Parkinson’s disease attributed to elevated tonic GABA discussed before is thought to arise from GAT downregulation on astrocytes.142 Given the role of microglia in synaptic pruning and its connection to neurotransmission defects in neurodegenerative disorders,149 there is also potential for microglia to contribute to observed defects in Parkinson’s disease.