Vulnerability of glia and vessels of rat substantia nigra in rotenone Parkinson model. (4th March 2018)

• Record Type: Journal Article
• Authors: Elgayar, Sanaa A. M.; Abdel-hafez, Amel A. M.; Gomaa, Asmaa M. S.; Elsherif, Raghda
• Is Part Of: Ultrastructural pathology. Volume 42:Number 2(2018)
• Page Start: 181
• Page End: 192
• Publication Date: 2018-03-04
• Subjects: Capillaries -- glia -- Parkinson model; Pathology, Cellular -- Periodicals; Ultrastructure (Biology) -- Periodicals; Diagnosis, Electron microscopic -- Periodicals; Microscopy, Electron; Pathology; 616.07582
• DOI: 10.1080/01913123.2017.1422066
• Languages: English
• ISSNs: 0191-3123

Abstract

ABSTRACT: Background : Astrocytes have been implicated as potentially exerting both neurotoxic and neuroprotective activities in Parkinson's disease (PD). Whether glial cells negatively impact the neuron integrity remains to be determined. We aimed to assess the vulnerability of glia and vessels in rat substantia nigra in a rotenone PD model.Material and Methods : Twenty adult male albino rats were divided into two equal groups: vehicle-control group (received dimethylsulfoxide + polyethylene glycol (PEG)-300, 1:1 v/v) and rotenone-treated group (received six doses of rotenone, 1.5 mg/kg/48 h s.c.). Using histological, ultrastructural, biochemical, and morphometric techniques, astrocytes, microglia, vessels, and total antioxidant capacity have been assessed.Results : The rotenone-treated group revealed an increase in the number of astrocytes compared to the control, conformational changes of the immature form, disruption of the outer mitochondrial membrane, and no increase in glial filaments. Dark microglia appeared in close vicinity of blood capillaries. The blood capillaries displayed an increase in number compared to the control, degenerated apoptotic endothelium, and pericytes and an increase in string vessels. The total antioxidant level significantly increased in rotenone-treated group ( p < 0.001) compared to the control group.Conclusion : Our results demonstrated that oxidative stress and mitochondrial dysfunction involved nigral cellular elements other than dopaminergic neurons. These included astrocytes, microglia, vascular endothelial cells, and pericytes, which might result in promoting damage to the neurons.