Modulation of Basal Ganglia Output from the SNr in Parkinson’s Disease & Levodopa-Induced Dyskinesia | NYU Langone Health

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Kang Lab Research Modulation of Basal Ganglia Output from the SNr in Parkinson’s Disease & Levodopa-Induced Dyskinesia

Modulation of Basal Ganglia Output from the SNr in Parkinson’s Disease & Levodopa-Induced Dyskinesia

The primary output structures of the basal ganglia are the globus pallidus interna (GPi) and substantia nigra reticulata (SNr), though the SNr is thought to play a more prominent role in rodents.  The GABAergic neurons of these nuclei integrate the activity of the direct and indirect striatal pathways to regulate important motor regions including the thalamus.  Combining neurophysiology with optogenetic and chemogenetic approaches, we are measuring how the activity of SNr changes in Parkinson’s disease and levodopa-induced dyskinesia models, how the direct modulation of SNr neurons alters the associated behavioral abnormalities, and how modulation of SNr neurons changes the activity of SNr target brain regions.

Panel A shows labelling SNr neurons in vivo by mCherry tag in DREAAD constructs introduced by AAV virus injection. B (mCherry control), C, and D panels show SNr neurons firing at higher rates due to DREAAD-hM3D-Gq (C) and lower rates due to DREAAD-hM4D-Gi expression (D) after CNO application in slice preparations.