Gray matter hypoxia in the brain of the experimental autoimmune encephalomyelitis model of multiple sclerosis
Date
2016-01-14
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Abstract
Background: Multiple sclerosis has a significant inflammatory component. As inflammation can induce and be modulated by hypoxia, the presence of hypoxia could provide clues about immune response regulation in MS.
Objective: quantify oxygenation in gray matter (GM) of mice with the experimental autoimmune encephalomyelitis (EAE) model to determine if hypoxia exists in a demyelination model associated with chronic inflammation.
Methods: C57BL/6 mice were implanted with a fiber-optic sensor in the cerebellum (n=13) and cortex (n=21). We measured PO2 in awake, unrestrained animals from baseline up to 36 days post-induction for EAE.
Results: There were more days with hypoxia compared with hyperoxia (cerebellum: 13/67 vs. 7/67 days; cortex: 15/112 vs. 2/112). Cerebellum showed the largest differences between days 13-17, corresponding to high behavioral deficits. This occurred later for cortex (day 23). Hypoxia in the cortex correlated with increased behavioral deficits and increased variation (based on z-score comparisons with baseline and age-matched controls) in the cerebellum correlated with clinical deficits.
Conclusions: The presence of hypoxia and increased variation in GM oxygenation indicates that oxygen may change enough to modulate the immune response. The cause may relate to increased metabolic dysfunction, disruption of neurovascular coupling or increased oxidative metabolism in activated microglia.
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This is the dataset for the paper whose abstract is included.
Keywords
Multiple Sclerosis, Experimental Autoimmune Encephalomyelitis, PO2, Hypoxia