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A new collaborative study from the Oxford Parkinson’s Disease Centre has revealed that GABA transporters on astrocytes, the brain's lesser known yet critically important cells, support dopamine release and are sites of early dysfunction in parkinsonism.

Showing striatal immunofluorescence signals for astrocyte marker S100β and neuronal marker NeuN
Striatal immunofluorescence signals for astrocyte marker S100β (magenta) and neuronal marker NeuN (yellow)

The release of the neurotransmitter dopamine in the brain region called the striatum plays key roles in both our motivation and how we select our actions. This release is dysregulated across diverse disorders including Parkinson's and various addictions. Unravelling the mechanisms by which dopamine release in the striatum is governed, and understanding how these mechanisms might be dysfunctional in disease, is critical for identifying novel targets for disease-modifying therapies.

A new study funded by Parkinson's UK and published in Nature Communications, led by Department of Physiology, Anatomy & Genetic's Professor Stephanie Cragg and Dr Bradley Roberts, and in collaboration with the Oxford Parkinson’s Disease Centre, uncovers new observations about how non-neuronal cells in the brain, namely astrocytes, regulate striatal dopamine release and are sites of early dysfunction in Parkinson’s.

The full story is available on the Department of Physiology, Anatomy & Genetics website

 

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