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Parkinson's disease is characterized by the progressive loss of midbrain dopamine neurons. Dopamine replacement therapy with levodopa alleviates parkinsonian motor symptoms but is complicated by the development of involuntary movements, termed levodopa-induced dyskinesia (LID). Aberrant activity in the striatum has been hypothesized to cause LID. Here, to establish a direct link between striatal activity and dyskinesia, we combine optogenetics and a method to manipulate dyskinesia-associated neurons, targeted recombination in active populations (TRAP). We find that TRAPed cells are a stable subset of sensorimotor striatal neurons, predominantly from the direct pathway, and that reactivation of TRAPed striatal neurons causes dyskinesia in the absence of levodopa. Inhibition of TRAPed cells, but not a nonspecific subset of direct pathway neurons, ameliorates LID. These results establish that a distinct subset of striatal neurons is causally involved in LID and indicate that successful therapeutic strategies for treating LID may require targeting functionally selective neuronal subtypes.
Pubmed ID: 29398356 RIS Download
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Seattle based independent, nonprofit medical research organization dedicated to accelerating the understanding of how human brain works. Provides free data and tools to researchers and educators and variety of unique online public resources for exploring the nervous system. Integrates gene expression data and neuroanatomy, along with data search and viewing tools, these resources are openly accessible via the Allen Brain Atlas data portal. Provides Allen Mouse Brain, Allen Spinal Cord Atlas, Allen Developing Mouse Brain Atlas, Allen Human Brain Atlas,Allen Mouse Brain Connectivity Atlas, Allen Cell Type Database, The Ivy Glioblastoma Atlas Project (Ivy GAP), The BrainSpan Atlas of the Developing Human Brain.
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