ArticleNeurochemical research2019
Increase in Glutamatergic Terminals in the Striatum Following Dopamine Depletion in a Rat Model of Parkinson's Disease.
Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- High-mobility Group Protein 1/ Receptor for Advanced Glycation End Products/ Nuclear Factor-κB Signalling Pathway Contributes to the Pathogenic Process of Striatal Neuron Impairment in the Rat Model of Parkinson's Disease.Brain and behavior · 2026Article
- Therapeutic Mechanisms of Exercise in Parkinson's Disease.International journal of molecular sciences · 2025Review
- Corticostriatal glutamate-mediated dynamic therapeutic efficacy of electroacupuncture in a parkinsonian rat model.Clinical and translational medicine · 2024Article
- Morphological changes in perisynaptic astrocytes induced by dopamine neuronal degeneration in the striatum of rats.Heliyon · 2024Article
- Inhibition of Vesicular Glutamate Transporters (VGLUTs) with Chicago Sky Blue 6B Before Focal Cerebral Ischemia Offers Neuroprotection.Molecular neurobiology · 2023Article
- A mini-review of the role of vesicular glutamate transporters in Parkinson's disease.Frontiers in molecular neuroscience · 2023Review
- Global, in situ analysis of the structural proteome in individuals with Parkinson's disease to identify a new class of biomarker.Nature structural & molecular biology · 2022Article
- Social defeat drives hyperexcitation of the piriform cortex to induce learning and memory impairment but not mood-related disorders in mice.Translational psychiatry · 2022Article
- Association Between Pathophysiological Mechanisms of Diabetic Retinopathy and Parkinson's Disease.Cellular and molecular neurobiology · 2022Review
- Comparative Ultrastructural Analysis of Thalamocortical Innervation of the Primary Motor Cortex and Supplementary Motor Area in Control and MPTP-Treated Parkinsonian Monkeys.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- VGLUT2 Is a Determinant of Dopamine Neuron Resilience in a Rotenone Model of Dopamine Neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- LY354740 Reduces Extracellular Glutamate Concentration, Inhibits Phosphorylation of Fyn/NMDARs, and Expression of PLK2/pS129 α-Synuclein in Mice Treated With Acute or Sub-Acute MPTP.Frontiers in pharmacology · 2020Article
- Research progress on the role of type I vesicular glutamate transporter (VGLUT1) in nervous system diseases.Cell & bioscience · 2020Review
- Thalamic degeneration in MPTP-treated Parkinsonian monkeys: impact upon glutamatergic innervation of striatal cholinergic interneurons.Brain structure & function · 2019Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Dopaminergic neuron degeneration is known to give rise to dendrite injury and spine loss of striatal neurons, however, changes of intrastriatal glutamatergic terminals and their synapses after 6-hydroxydopamine (6OHDA)-induced dopamine (DA)-depletion remains controversial. To confirm the effect of striatal DA-depletion on the morphology and protein levels of corticostriatal and thalamostriatal glutamatergic terminals and synapses, immunohistochemistry, immuno-electron microscope (EM), western blotting techniques were performed on Parkinson's disease rat models in this study. The experimental results of this study showed that: (1) 6OHDA-induced DA-depletion resulted in a remarkable increase of Vesicular glutamate transporter 1 (VGlut1) + and Vesicular glutamate transporter 2 (VGlut2)+ terminal densities at both the light microscope (LM) and EM levels, and VGlut1+ and VGlut2+ terminal sizes were shown to be enlarged by immuno-EM; (2) Striatal DA-depletion resulted in a decrease in both the total and axospinous terminal fractions of VGlut1+ terminals, but the axodendritic terminal fraction was not significantly different from the control group. However, total, axospinous and axodendritic terminal fractions for VGlut2+ terminals declined significantly after striatal DA-depletion. (3) Western blotting data showed that striatal DA-depletion up-regulated the expression levels of the VGlut1 and VGlut2 proteins. These results suggest that 6OHDA-induced DA-depletion affects corticostriatal and thalamostriatal glutamatergic synaptic inputs, which are involved in the pathological process of striatal neuron injury induced by DA-depletion.
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