Healthcare (Commonwealth Union) – The role of dopamine in a variety of conditions has been well documented and studied. High or excessive dopamine has been linked to manic episodes in conditions such as bipolar disorder and schizophrenia which can manifest with hallucinations, irrational behavior along with confusion. Lower dopamine levels have been linked to depression along with a variety of other conditions. The role of the D2 receptor has been much in focus together with the role of antipsychotics in stabilizing dopamine levels.
New findings are reshaping scientific understanding of Parkinson’s disease. Preclinical research indicates that movement depends on a consistent supply of dopamine, offering insight into why existing therapies are effective and how they might be refined.
A study led by researchers at McGill University questions a long-held belief about dopamine’s role in controlling movement, a shift that could influence future approaches to treating Parkinson’s disease.
Published in Nature Neuroscience, the study suggests dopamine does not directly regulate the speed or strength of individual movements, as previously assumed. Instead, it functions as a foundational mechanism that enables movement to occur at all.
“Our findings suggest we should rethink dopamine’s role in movement,” explained the senior author Nicolas Tritsch, Assistant Professor in McGill’s Department of Psychiatry and researcher at the Douglas Research Centre. “Restoring dopamine to a normal level may be enough to improve movement. That could simplify how we think about Parkinson’s treatment.”
Dopamine has long been recognised as crucial for motor vigour — the capacity to move with speed and force. In people with Parkinson’s disease, the loss of dopamine-producing neurons results in slowed movements, tremors, and problems with balance.
Levodopa, the most common treatment for Parkinson’s, improves mobility, yet the precise reason it is effective has remained unclear. More recently, sophisticated techniques have revealed brief bursts of dopamine during movement, leading researchers to suggest that these surges regulate motor vigour.
The latest research challenges that idea.
Tritsch indicated that instead of serving as a throttle that controls how fast movements are performed, dopamine seems to play a role similar to engine oil and it keeps the system functioning properly, but it does not dictate the speed of individual actions.
The scientists gaged brain activity in mice as a weighted lever was pressed, turning dopamine cells “on” or “off” with the utilization of a light-based technique.
If fast dopamine bursts did control vigour, changing dopamine at that moment should have made movements faster or slower. To their surprise, it had no effect. In tests with levodopa, they found the medication worked by boosting the brain’s baseline level of dopamine, not by restoring the fast bursts.
A more precise target for treatment from the researchers of the study. More than 110,000 Canadians live with Parkinson’s disease, a number projected to more than double by 2050 as the population ages.
Researchers of the study indicated that a more accurate explanation for the reason levodopa is effective paves the way for new therapies designed to retain baseline dopamine levels, according to the authors.
Tracking dopamine in real time was a key component of the study. The discovery also prompts a re-evaluation of established treatments. Dopamine receptor agonists have demonstrated potential benefits, but their widespread action across the brain led to unwanted side effects. This new insight gives researchers clearer guidance on how to develop more targeted and safer alternatives.
The study titled “Subsecond dopamine fluctuations do not specify the vigor of ongoing actions” appeared in Nature Neuroscience.
The research received financial support from the Canada First Research Excellence Fund, provided through McGill University’s Healthy Brains, Healthy Lives initiative, as well as from the Fonds de Recherche du Québec.
