Differential Effects of LPS and 6-OHDA on Microglia’s Morphology in Rats: Implications for Inflammatory Model of Parkinson’s Disease

被引:0
作者
Irving Parra
Isabel Martínez
Gabriel Ramírez-García
Yousef Tizabi
Liliana Mendieta
机构
[1] Benemérita Universidad Autónoma de Puebla,Laboratorio de Neuroquímica, Facultad de Ciencias Químicas
[2] Universidad Nacional Autónoma de México,Unidad Periférica de Neurociencias, Facultad de Medicina
[3] Instituto Nacional de Neurología y Neurocirugía “Manuel Velasco Suárez”,Department of Pharmacology
[4] Howard University College of Medicine,undefined
来源
Neurotoxicity Research | 2020年 / 37卷
关键词
6-Hydroxydopamine; Lipopolysaccharide; Microglia; Substantia nigra; Parkinson’s disease; Inflammation;
D O I
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摘要
Parkinson’s disease (PD) is an idiopathic and progressive neurodegenerative disease characterized by the loss of ~ 80% of dopaminergic neurons in substantia nigra pars compacta (SNpc). Because activation of the innate cellular immune response, mediated by microglia, has been linked to the neurodegeneration in PD, in the present study, we evaluated the effects of lipopolysaccharide (LPS) and 6-hydroxydopamine (6-OHDA) on microglia’s morphology, reflective of their activity, as well as tyrosine hydroxylase (TH)-positive neurons in SNpc and motor behavior. Adult male Wistar rats were stereotactically injected with LPS or 6-OHDA into the left dorsolateral striatum. Control groups received appropriate vehicle. The morphological changes of microglial cells and neurotoxic effects were examined at 1, 7, and 14 post-injection days. Both LPS and 6-OHDA caused activation and morphological changes in microglial cells as well as loss of dopaminergic neurons in SNpc. These effects were maximal at 14 days post-injection where motor impairments were also evident. However, our findings indicate that 6-OHDA causes a low degree of microglia activation compared to LPS. Hence, it may be concluded that LPS model of PD might be a better representation of inflammatory involvement in this devastating disease.
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页码:1 / 11
页数:10
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