Parkinson's disease, a progressive neurodegenerative disorder, results from the death of cells in various parts of the brain, especially in a region called the substantia nigra.

It is in the substantia nigra that a neurotransmitter called dopamine is formed, and when dopamine is lacking neurons fire abnormally, impairing one's ability to control movement.

While Parkinson's is not curable, it is treatable with L-DOPA, which is converted into dopamine in the brain. However, while taking L-DOPA helps patients move normally, in many individuals it eventually triggers uncontrolled excessive movements called dyskinesia.

Most studies into the cause of dyskinesia in Parkinson's have focused on the dopamine receptors that remain in the brain, which over time become over-reactive to L-DOPA therapy. However, the researchers in the paper published in the journal Neuron decided to look at how neurons of the basal ganglia regulates movement in the absence of dopamine.

They found that after long-term dopamine loss, striatonigral neurons lose their ability to respond to the neurotransmitter GABA (gamma-aminobutyric acid). This effect was not found with short-term dopamine loss.

"When striatonigral neurons are working normally, they act as a brake on the basal ganglia, in effect shutting down unwanted movement," said the author. "But when there is dopamine loss, as in Parkinson's, striatonigral neurons try to compensate, and eventually lose their responsiveness to GABA. Our hypothesis is that when L-DOPA is added into the system, you lose the ability to filter, or turn off, unwanted movement."