summary: The new findings suggest that Parkinson’s disease may develop silently for more than a decade before symptoms appear. The study found that the brain’s motor circuits can maintain their function even with a sharp decrease in active dopamine secretion, a phenomenon that contradicts popular belief.
Dopamine is crucial for movement, and its deficiency is a hallmark of Parkinson’s disease. These findings could pave the way for new therapeutic approaches to alleviate the symptoms of this neurological disease.
Key facts:
- The research indicates that Parkinson’s disease may progress for more than 10 years without symptoms.
- The brain’s motor circuits have been found to be surprisingly flexible, functioning normally even with an almost complete loss of active dopamine secretion.
- These findings could lead to new ways to treat symptoms of Parkinson’s disease by understanding the mechanisms involved in the release of dopamine in the brain.
source: University of Montreal
Have you or someone close to you been diagnosed with Parkinson’s disease? Well, chances are the disease has been progressing quietly but insidiously for more than 10 years, new research shows.
Conducted at the University of Montreal and published in the journal Nature CommunicationsThe research sheds new light on the surprising plasticity of the brain during a period without symptoms of Parkinson’s disease.
In their study, a team led by Louis-Eric Trudeau, a neuroscientist at UdeM, showed that the motor circuits in the brains of mice are insensitive to an almost complete loss of active secretion of this chemical messenger.
This observation is surprising because dopamine is a chemical messenger known to be important in movement. And in Parkinson’s disease, dopamine levels in the brain drop relentlessly.
said Trudeau, a professor in the department of pharmacology and the department of physiology and neurosciences.
Using genetic manipulation, Trudeau and his researchers removed the ability of dopamine-producing neurons to release this chemical messenger in response to the normal electrical activity of these cells.
As a doctoral student in Trudeau’s lab, Benoit Dilignat-Lavaud predicted a loss of motor function in these mice similar to what is seen in individuals with Parkinson’s disease.
But surprise! The mice showed a completely normal ability to move.
Measurement of dopamine levels
Meanwhile, measurements of total brain dopamine levels, conducted by UdeM traumatologist Louis de Beaumont’s team at the Research Center at the Hospital Sacré-Cœur de Montréal, revealed that extracellular dopamine levels in the brains of these mice were normal.
These results indicate that the activity of the motor circuits in the brain requires only low basal dopamine levels.
It is therefore likely that in the early stages of Parkinson’s disease, basal dopamine levels in the brain remain high enough for many years – this is, despite the gradual loss of dopamine-producing neurons. Motor disturbances appear only when the threshold is exceeded.
According to the scientists, by identifying the mechanisms involved in dopamine release in the brain, this advance in Parkinson’s disease research could help identify new ways to reduce symptoms of this intractable neurodegenerative disease.
About Research News on Parkinson’s Disease
author: Jeff Heinrich
source: University of Montreal
communication: Jeff Heinrichs – University of Montreal
picture: Image credited to Neuroscience News
Original search: open access.
“Synaptotagmin-1-dependent axonal dopamine release can be mediated in baseline locomotor behaviors in ratsBy Louis Eric Trudeau et al. Nature Communications
a summary
Synaptotagmin-1-dependent axonal dopamine release can be mediated in baseline locomotor behaviors in rats
In Parkinson’s disease (PD), motor dysfunction does not appear until after severe loss of DA innervation. It has been hypothesized that this flexibility is due to the ability of many motor behaviors to be sustained by a diffuse basal tone of the DA; But empirical evidence for this is limited.
Here we show that conditional deletion of the calcium sensor synaptotagmin-1 (Syt1) in DA neurons (Syt1 cKODA mice) abolishes most activity-dependent axonal DA release in the striatum and midbrain, leaving DA release (STD) intact.
Strikingly, Syt1 cKODA The rats showed intact performance in several unconditioned DA-dependent motor tasks and even in the task of evaluating the conditioned drive for food.
Given that basal extracellular DA levels in the striatum were unaltered, our results indicate that activity-dependent DA release is dispensable for such tasks and that it may be maintained by basal tone of extracellular DA.
Taken together, our findings reveal the striking plasticity of DA-dependent motor functions in a peri-abrogation context of phasic DA firing, shedding new light on why widespread loss of DA innervation is needed to detect motor dysfunction in PD.
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