Regulating astrocytic activity in the dorsal striatum mitigates L-dopa-induced dyskinesia in Parkinson’s disease

Abstract In Parkinson’s disease (PD), long-term 3,4-dihydroxy-L-phenylalanine (L-dopa) therapy leads to the development of motor complications, including L-dopa-induced dyskinesia (LID). Increased numbers of reactive astrocytes in the brains of patients with PD are a key feature of this disease. Ast...

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Main Authors: Young-Kyoung Ryu, Hye-Yeon Park, Ju-Eun Kim, Hyun-Hee Seo, Chul-Ho Lee, Kyoung-Shim Kim
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-12104-5
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author Young-Kyoung Ryu
Hye-Yeon Park
Ju-Eun Kim
Hyun-Hee Seo
Chul-Ho Lee
Kyoung-Shim Kim
author_facet Young-Kyoung Ryu
Hye-Yeon Park
Ju-Eun Kim
Hyun-Hee Seo
Chul-Ho Lee
Kyoung-Shim Kim
author_sort Young-Kyoung Ryu
collection DOAJ
description Abstract In Parkinson’s disease (PD), long-term 3,4-dihydroxy-L-phenylalanine (L-dopa) therapy leads to the development of motor complications, including L-dopa-induced dyskinesia (LID). Increased numbers of reactive astrocytes in the brains of patients with PD are a key feature of this disease. Astrocytes are involved in the development of LID; however, whether the regulation of astrocytic activity influences LID development remains unclear. Therefore, this study aimed to determine the effect of the direct modulation of glial fibrillary acidic protein (GFAP)-expressing glia on LID development during L-dopa therapy in PD using chemogenetic tools. Adeno-associated viruses (AAVs) were used to target designer receptors exclusively activated by designer drugs (DREADDs) in GFAP-expressing cells to modulate Gq- or Gi-mediated signaling and regulate astrocytic activity in the brain. AAVs were injected into the dorsal striatum, and 6-hydroxydopamine (6-OHDA) was injected into the substantia nigra of mice. Clozapine N-oxide was co-administered with L-dopa. Chemogenetic activation of astrocytes in the dopamine-depleted striatum affected the early development of LID in 6-OHDA-lesioned mice. Furthermore, astrocyte suppression through Gi-mediated DREADD reduced abnormal involuntary movement scores in mice. These results suggest that regulating astrocytic activity in the dorsal striatum could be a therapeutic option for LID in PD.
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spelling doaj-art-9d4b8d8a59e741849054d9f1e7f8d54a2025-08-20T04:03:06ZengNature PortfolioScientific Reports2045-23222025-07-0115111210.1038/s41598-025-12104-5Regulating astrocytic activity in the dorsal striatum mitigates L-dopa-induced dyskinesia in Parkinson’s diseaseYoung-Kyoung Ryu0Hye-Yeon Park1Ju-Eun Kim2Hyun-Hee Seo3Chul-Ho Lee4Kyoung-Shim Kim5Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)Abstract In Parkinson’s disease (PD), long-term 3,4-dihydroxy-L-phenylalanine (L-dopa) therapy leads to the development of motor complications, including L-dopa-induced dyskinesia (LID). Increased numbers of reactive astrocytes in the brains of patients with PD are a key feature of this disease. Astrocytes are involved in the development of LID; however, whether the regulation of astrocytic activity influences LID development remains unclear. Therefore, this study aimed to determine the effect of the direct modulation of glial fibrillary acidic protein (GFAP)-expressing glia on LID development during L-dopa therapy in PD using chemogenetic tools. Adeno-associated viruses (AAVs) were used to target designer receptors exclusively activated by designer drugs (DREADDs) in GFAP-expressing cells to modulate Gq- or Gi-mediated signaling and regulate astrocytic activity in the brain. AAVs were injected into the dorsal striatum, and 6-hydroxydopamine (6-OHDA) was injected into the substantia nigra of mice. Clozapine N-oxide was co-administered with L-dopa. Chemogenetic activation of astrocytes in the dopamine-depleted striatum affected the early development of LID in 6-OHDA-lesioned mice. Furthermore, astrocyte suppression through Gi-mediated DREADD reduced abnormal involuntary movement scores in mice. These results suggest that regulating astrocytic activity in the dorsal striatum could be a therapeutic option for LID in PD.https://doi.org/10.1038/s41598-025-12104-5Abnormal involuntary movementsStriatumAAV-GFAP-hM3D(Gq)AAV-GFAP-hM4D(Gi)Clozapine N-oxide (CNO)6-hydroxydopamine-induced mouse model
spellingShingle Young-Kyoung Ryu
Hye-Yeon Park
Ju-Eun Kim
Hyun-Hee Seo
Chul-Ho Lee
Kyoung-Shim Kim
Regulating astrocytic activity in the dorsal striatum mitigates L-dopa-induced dyskinesia in Parkinson’s disease
Scientific Reports
Abnormal involuntary movements
Striatum
AAV-GFAP-hM3D(Gq)
AAV-GFAP-hM4D(Gi)
Clozapine N-oxide (CNO)
6-hydroxydopamine-induced mouse model
title Regulating astrocytic activity in the dorsal striatum mitigates L-dopa-induced dyskinesia in Parkinson’s disease
title_full Regulating astrocytic activity in the dorsal striatum mitigates L-dopa-induced dyskinesia in Parkinson’s disease
title_fullStr Regulating astrocytic activity in the dorsal striatum mitigates L-dopa-induced dyskinesia in Parkinson’s disease
title_full_unstemmed Regulating astrocytic activity in the dorsal striatum mitigates L-dopa-induced dyskinesia in Parkinson’s disease
title_short Regulating astrocytic activity in the dorsal striatum mitigates L-dopa-induced dyskinesia in Parkinson’s disease
title_sort regulating astrocytic activity in the dorsal striatum mitigates l dopa induced dyskinesia in parkinson s disease
topic Abnormal involuntary movements
Striatum
AAV-GFAP-hM3D(Gq)
AAV-GFAP-hM4D(Gi)
Clozapine N-oxide (CNO)
6-hydroxydopamine-induced mouse model
url https://doi.org/10.1038/s41598-025-12104-5
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