XXXX release influences @entity2657 formation after diffuse @entity131 .

@entity11095 @entity32 @entity131 @entity2657 @entity2951 @entity130 @entity4 @entity73 @entity51 @entity35 @entity13624
The mechanisms associated with @entity4 formation after @entity131 ( @entity131 ) have not been fully elucidated. In peripheral tissue injury, the neurogenic component of @entity32 plays a significant role in increased vascular permeability and @entity4 formation. However, few studies have examined the role of @entity11095 induced @entity13624 following @entity131 . Adult male @entity35 were either left untreated, or pre-treated with @entity2951 (125 mg/kg s.c.) or equal volume vehicle, and injured 14 days later using the 2-meter impact-acceleration model. Subgroups of animals were assessed for blood brain barrier (BBB) permeability (Evans Blue), @entity2657 (wet weight/dry weight) and functional outcome (Barnes maze and Rotarod) for up to 2 weeks post- @entity130 . Increased BBB permeability was present in untreated animals between 3 and 6 h after injury but not at later time-points. @entity4 was maximal at 5 h after @entity130 , declined and then significantly increased over the 5 days post- @entity130 . In contrast, @entity2951 pre-treated, @entity11095 -depleted animals exhibited no significant increase in BBB permeability or @entity4 compared to vehicle treated animals after injury. Notably, motor and @entity73 were significantly reduced in the @entity2951 -pretreated animals. We conclude that @entity13624 contributes to the development of @entity4 and @entity51 after diffuse @entity131 .
