Differential vulnerability of oligodendrocytes and astrocytes to hypoxic–ischemic stresses

Marrif, Husnia; Juurlink, Bernhard H.J.

doi:10.1016/s1569-2558(03)31037-9

Cited by 4 publications

(2 citation statements)

References 62 publications

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“…Neuron sparing in the face of mitochondrial stress imposed by CPZ has been explained by metabolic coupling to astrocytes, which augment neuronal resilience by carrying out glycolysis in response to energetic deficits (Dewar et al, 2003; Marrif and Juurlink, 2003; Praet et al, 2014). In addition to increased numbers of GFAP + reactive astrocytes, astrocytes displayed crossed domains, membrane blebbing, upregulation of GFAP, and altered AQP4 expression with chronic demyelination concurrent with changes to theta and beta frequency power and spontaneous seizure.…”

Section: Discussionmentioning

confidence: 99%

Chronic demyelination-induced seizures

et al. 2017

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Multiple sclerosis (MS) patients are three to six times more likely to develop epilepsy compared to the rest of the population. Seizures are more common in patients with early onset or progressive forms of the disease and prognosticate rapid progression to disability and death. Grey matter atrophy, hippocampal lesions, interneuron loss, and elevated juxtacortical lesion burden have been identified in MS patients with seizures; however, translational studies aimed at elucidating the pathophysiological processes underlying MS epileptogenesis are limited. Here, we report that cuprizone-mediated chronically demyelinated (9-12 weeks) mice exhibit marked changes in electroencephalography (EEG) and evidence of overt seizure activity in mice. Subsequently, histopathological correlates were probed by immunohistochemistry, revealing extensive demyelination, loss of parvalbumin inhibitory interneurons in the hippocampus CA1 subregion, widespread gliosis and changes to astrocytic aquaporin-4 expression. Our results suggest that chronically demyelinated mice are a valuable model with which we may begin to understand the mechanisms underlying demyelination-induced seizures.

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Section: Discussionmentioning

confidence: 99%

Chronic demyelination-induced seizures

et al. 2017

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“…However, hypoxic condition in the white matter did not induce responses of oligodendrocytes, as well as no anti-oxidant responses. 30 Astrocytes are the most abundant subtypes of glial cells which provide many functions, including structural support, metabolism, maintenance of the extracellular environment, regulation of blood flow, stabilization of cell-cell communication and defence against oxidative stress. 31 In the white matter fibrous astrocytes have physical contact with oligodendrocytes and play crucial role in support of the white matter.…”

Section: Discussionmentioning

confidence: 99%

Bradykinin and noradrenaline preconditioning influences level of antioxidant enzymes SOD, CuZn-SOD, Mn-SOD and catalase in the white matter of spinal cord in rabbits after ischemia/reperfusion

et al. 2019

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The aim of present work is to assess the effects of bradykinin (Br) or noradrenaline (Nor) preconditioning to the levels of antioxidant enzymes: superoxide dismutase (SOD), copper, zinc superoxide dismutase (CuZn-SOD), manganese superoxide dismutase (Mn-SOD) and catalase in ischemia/reperfusion (I/R) model in the rabbit spinal cord white matter as well as effect on glial fibrillary acidic protein (GFAP) and ubiquitin immunoreaction in glial cells. Rabbits were preconditioned by intraperitoneal single dose of Br or Nor 48 h prior to 20 min of ischemia followed by 24 or 48 h of reperfusion. White matter of L3-L6 spinal cord segments was used for comparison of antioxidant enzyme levels in sham control, ischemic groups and four preconditioned groups. The total SOD level in the Br or Nor preconditioned groups after 48 h of reperfusion was increased vs Br or Nor preconditioned groups after 24 h of reperfusion. The comparison among the ischemic group vs Br preconditioned (P<0.05), and Nor preconditioned (P<0.001) groups after 48 h of reperfusion, showed statistically significant decrease of Mn-SOD activity. Tissue catalase level activity was significantly decreased in the Br preconditioned group after 48 h of reperfusion (P<0.05) and Nor preconditioned groups after 24 h of reperfusion (P<0.001) and also after 48 h of reperfusion (P<0.001), in comparison to ischemic group after 48 h of reperfusion. Significantly decreased tissue catalase activity (P<0.05) in both Nor preconditioned groups after 24 or 48 h of reperfusion was measured vs Br preconditioned group after 48 h of reperfusion. According to our results, in the white matter, activation of stress proteins in glial cells, as well as antioxidant enzymes levels, were influenced by pharmacological preconditioning followed by 20 min of ischemia and 24 or 48 h of reperfusion. These changes contribute to ischemic tolerance acquisition and tissue protection from oxidative stress during reperfusion period.

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Oxidative Stress and Neurodegeneration

Pasquini

Quintá

2016

Biochemistry of Oxidative Stress

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Differential vulnerability of oligodendrocytes and astrocytes to hypoxic–ischemic stresses

Cited by 4 publications

References 62 publications

Chronic demyelination-induced seizures

Chronic demyelination-induced seizures

Bradykinin and noradrenaline preconditioning influences level of antioxidant enzymes SOD, CuZn-SOD, Mn-SOD and catalase in the white matter of spinal cord in rabbits after ischemia/reperfusion

Oxidative Stress and Neurodegeneration

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