Researchers
working in the lab of Carnegie Mellon University neuroscientist Aryn Gittis,
have identified two groups of neurons that can be turned on and off to
alleviate the movement-related symptoms of Parkinson's disease. The activation
of these cells in the basal ganglia relieves symptoms for much longer than
current therapies, like deep brain stimulation and pharmaceuticals.
The
study, completed in a mouse model
of Parkinson's, used optogenetics to better understand the neural circuitry
involved in Parkinson's disease, and could provide the basis for new
experimental treatment protocols. The findings, published by researchers from
Carnegie Mellon, the University of Pittsburgh and the joint CMU/Pitt Center for
the Neural Basis of Cognition (CNBC) are available as an Advance Online
Publication on Nature Neuroscience's website.
Parkinson's
disease is caused when the dopamine neurons
that feed into the brain's basal ganglia die and
cause the basal ganglia
to stop working, preventing the body from initiating voluntary movement. The
basal ganglia is the main clinical target for treating Parkinson's disease, but
currently used therapies do not offer long-term solutions.
"A
major limitation of Parkinson's disease treatments is that they provide
transient relief of symptoms. Symptoms can return rapidly if a drug dose is
missed or if deep brain
stimulation is discontinued," said Gittis, assistant professor
of biological sciences in the Mellon College of Science and member of Carnegie
Mellon's BrainHub neuroscience initiative and the CNBC. "There is no
existing therapeutic strategy for long lasting relief of movement disorders
associated with Parkinson's."
To
better understand how the neurons in the basal ganglia behave in Parkinson's,
Gittis and colleagues looked at the inner circuitry of the basal ganglia. They
chose to study one of the structures that makes up that region of the brain, a
nucleus called the external globus pallidus (GPe). The GPe is known to
contribute to suppressing motor pathways in the basal ganglia, but little is
known about the individual types of neurons present in the GPe, their role in
Parkinson's disease or their therapeutic potential.
The
research group used optogenetics, a technique that turns genetically tagged
cells on and off with light. They targeted two cell types in a mouse model for
Parkinson's disease: PV-GPe neurons and Lhx6-GPe neurons. They found that by
elevating the activity of PV-GPe neurons over the activity of the Lhx6-GPe neurons, they were able to
stop aberrant neuronal behavior in the basal ganglia and restore movement in
the mouse model for at least four hours—significantly longer than current
treatments.
While
optogenetics is used only in animal models, Gittis said she believes their
findings could create a new, more effective deep brain stimulation protocol.
More
information: Cell-specific pallidal intervention induces
long-lasting motor recovery in dopamine-depleted mice, Nature Neuroscience
(2017). nature.com/articles/doi:10.1038/nn.4559
Journal reference: Nature
Neuroscience
Provided by: Carnegie Mellon
University
https://medicalxpress.com/news/2017-05-neuronal-movement-parkinson-disease.html
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