Joe C. Brague

Transiently-elevated dopamine triggers plasticity that preserves motor function, striatal neuron morphology, and thalamostriatal input in a mouse model of Parkinson's disease

The paper shows that temporarily increasing dopamine in a Parkinson's mouse model preserves motor function, neuron structure, and specific neural inputs.

A striatal plasticity that supports the long-term preservation of motor function in Parkinsonian mice.

This study identifies a striatal plasticity mechanism that delays motor deficits in a Parkinsonian mouse model by preserving direct pathway connectivity through transient dopamine neuron activity elevation.