ArticleNeural regeneration research2020
Characteristic response of striatal astrocytes to dopamine depletion.
Article in Neural regeneration research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Trial
- Inhibiting the transient receptor potential melastatin 2 channel in microglia: current evidence and therapeutic potential in neurological disorders.Acta pharmacologica Sinica · 2026Review
- Research progress on the role of exercise-regulated reactive astrocytes in the prevention and treatment of Parkinson's disease.Frontiers in aging neuroscience · 2025Review
- Morphological changes in perisynaptic astrocytes induced by dopamine neuronal degeneration in the striatum of rats.Heliyon · 2024Article
- Glial cells improve Parkinson's disease by modulating neuronal function and regulating neuronal ferroptosis.Frontiers in cell and developmental biology · 2024Review
- Systems level analysis of sex-dependent gene expression changes in Parkinson's disease.NPJ Parkinson's disease · 2023Article
- Trafficking of the glutamate transporter is impaired in LRRK2-related Parkinson's disease.Acta neuropathologica · 2022Article
- Role of JAK-STAT and PPAR-Gamma Signalling Modulators in the Prevention of Autism and Neurological Dysfunctions.Molecular neurobiology · 2022Review
- Inhibition of TRPM2 by AG490 Is Neuroprotective in a Parkinson's Disease Animal Model.Molecular neurobiology · 2022Article
- Alpha-Synuclein as a Prominent Actor in the Inflammatory Synaptopathy of Parkinson's Disease.International journal of molecular sciences · 2021Review
- Neuroprotective and Anti-Inflammatory Effects of Evernic Acid in an MPTP-Induced Parkinson's Disease Model.International journal of molecular sciences · 2021Article
- Alterations in dopamine system and in its connectivity with serotonin in a rat model of Alzheimer's disease.Brain communications · 2021Article
- Review
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8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Astrocytes and astrocyte-related proteins play important roles in maintaining normal brain function, and also regulate pathological processes in brain diseases and injury. However, the role of astrocytes in the dopamine-depleted striatum remains unclear. A rat model of Parkinson's disease was therefore established by injecting 10 μL 6-hydroxydopamine (2.5 μg/μL) into the right medial forebrain bundle. Immunohistochemical staining was used to detect the immunoreactivity of glial fibrillary acidic protein (GFAP), calcium-binding protein B (S100B), and signal transducer and activator of transcription 3 (STAT3) in the striatum, and to investigate the co-expression of GFAP with S100B and STAT3. Western blot assay was used to measure the protein expression of GFAP, S100B, and STAT3 in the striatum. Results demonstrated that striatal GFAP-immunoreactive cells had an astrocytic appearance under normal conditions, but that dopamine depletion induced a reactive phenotype with obvious morphological changes. The normal striatum also contained S100B and STAT3 expression. S100B-immunoreactive cells were uniform in the striatum, with round bodies and sparse, thin processes. STAT3-immunoreactive cells presented round cell bodies with sparse processes, or were darkly stained with a large cell body. Dopamine deprivation induced by 6-hydroxydopamine significantly enhanced the immunohistochemical positive reaction of S100B and STAT3. Normal striatal astrocytes expressed both S100B and STAT3. Striatal dopamine deprivation increased the number of GFAP/S100B and GFAP/STAT3 double-labeled cells, and increased the protein levels of GFAP, S100B, and STAT3. The present results suggest that morphological changes in astrocytes and changes in expression levels of astrocyte-related proteins are involved in the pathological process of striatal dopamine depletion. The study was approved by Animal Care and Use Committee of Sun Yat-sen University, China (Zhongshan Medical Ethics 2014 No. 23) on September 22, 2014.
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