Gray matter hypoxia in the brain of the experimental autoimmune encephalomyelitis model of multiple sclerosis

Johnson, Thomas W.; Dunn, Jeff F.; Wu, Ying; Nathoo, Nabeela; Rogers, James A.; Yong, V. Wee

Gray matter hypoxia in the brain of the experimental autoimmune encephalomyelitis model of multiple sclerosis

dc.contributor.author	Johnson, Thomas W.
dc.contributor.author	Dunn, Jeff F.
dc.contributor.author	Wu, Ying
dc.contributor.author	Nathoo, Nabeela
dc.contributor.author	Rogers, James A.
dc.contributor.author	Yong, V. Wee
dc.date.accessioned	2016-01-13T20:19:50Z
dc.date.available	2016-01-13T20:19:50Z
dc.date.issued	2016-01-14
dc.description	This is the dataset for the paper whose abstract is included.	en_US
dc.description.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.	en_US
dc.description.grantingagency	NSERC; CIHR; AIHS; CFI; endMS	en_US
dc.description.refereed	No	en_US
dc.identifier.doi	http://dx.doi.org/10.11575/PRISM/10690
dc.identifier.uri	http://hdl.handle.net/1880/51061
dc.language.iso	en_US	en_US
dc.publisher.institution	University of Calgary	en_US
dc.subject	Multiple Sclerosis	en_US
dc.subject	Experimental Autoimmune Encephalomyelitis	en_US
dc.subject	PO2	en_US
dc.subject	Hypoxia	en_US
dc.title	Gray matter hypoxia in the brain of the experimental autoimmune encephalomyelitis model of multiple sclerosis	en_US
dc.type	dataset	en_US