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- 저자 : Poornima D. E. Weerasinghe-Mud (검색결과 2 건)
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Acute MPTP treatment impairs dendritic spine density in the mouse hippocampus
Poornima D. E. Weerasinghe-Mud,Mary Jasmin Ang,Mai Wada,Sung-Ho Kim,Taekyun Shin,Miyoung Yang,Changjong Moon 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
Among the animal models of Parkinson"s disease (PD), the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse model has shown both dopaminergic (DA) damage and related motor control defects, as observed in patients with PD. Recent studies have suggested that the DA system interacts with the synaptic plasticity of the hippocampus in PD. However, little is known about how alterations in the hippocampal structural plasticity are affected by the DA damage in MPTP-lesioned models. In the present study, we investigated alterations in dendritic complexity and spine density in the mouse hippocampus following acute MPTP treatment (22 mg/kg, i.p., four times/day, 2-h intervals). We confirmed that acute MPTP treatment significantly decreased initial motor function and reduced persistently the number of tyrosine hydroxylase-positive DA neurons in the substantia nigra. Golgi staining showed that acute MPTP treatment significantly reduced the spine density of neuronal dendrites in the cornu ammonis 1 (CA1) apical/basal and dentate gyrus (DG) subregions of the mouse hippocampus at 8 and 16 days after treatment, although it did not affect dendritic complexity (e.g., number of crossing dendrites, total dendritic length, and branch points per neuron) in both CA1 and DG subregions at all time points after treatment. Therefore, the present study provides anatomical evidence that acute MPTP treatment affects synaptic structure in the hippocampus during the late phase after acute MPTP treatment in mice, independent of any changes in the dendritic arborization of hippocampal neurons. These findings offer data for the ability of the acute MPTP-lesioned mouse model to replicate the non-nigrostriatal lesions of clinical PD.
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Meejung Ahn,Poornima D. E. Weerasinghe-Mud,Hyobin Kim,Minju Kwon,Jeongtae Kim,Taekyun Shin 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
Progranulin (PGRN) which is a secreted neurotrophin mediates cell cycle progression and cell motility that contribute to MHC-mediated antigen processing, pathogen removal, and autoimmunity. To evaluate the involvement of PGRN in experimental autoimmune neuritis (EAN) pathogenesis, as a model of human demyelinating diseases such as Guillain- Barré Syndrome. The expression of PGRN in rat sciatic nerves with EAN was studied. PGRN expression was increased significantly in EAN-affected sciatic nerves compared with normal rat sciatic nerves. The elevated levels of PGRN in the sciatic nerves of rats with EAN at the peak stage and then its expression was decreased significant at the recovery stage. The cellular phenotype of PGRN in EAN lesions consisted mainly of inflammatory cells including macrophages and Schwann cells whereas it was expressed constitutively in axons. Collectively, this study suggests that PGRN secreted by a variety of cells including macrophage, vascular endothelial cells and Schwann cells, plays either pro-inflammatory or tissue regenerative effects, or both depending on PGRN containing cell type, during the course of EAN, an animal model of human demyelinating disease. (Acknowledgement: This work was supported by the National Research Foundation of Korea: Grant number NRF-2017R1A2B4012478)
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