Increase in Glutamatergic Terminals in the Striatum Following Dopamine Depletion in a Rat Model of Parkinson’s Disease
Autor: | Xuefeng Zheng, Yanmei Li, Zhi Chen, Ziyun Huang, Bingbing Liu, Yaofeng Zhu, Linju Jia, Wanlong Lei, Tao Chen |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Parkinson's disease Vesicular glutamate transporter 1 Dendrite Striatum Biochemistry 03 medical and health sciences Cellular and Molecular Neuroscience Glutamatergic 0302 clinical medicine Dopamine Internal medicine medicine biology Chemistry General Medicine medicine.disease Blot 030104 developmental biology Endocrinology medicine.anatomical_structure biology.protein Immunohistochemistry 030217 neurology & neurosurgery medicine.drug |
Zdroj: | Neurochemical Research. 44:1079-1089 |
ISSN: | 1573-6903 0364-3190 |
Popis: | 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. |
Databáze: | OpenAIRE |
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