Fig. 3.

Chronic consequences of post-injury (±)-rolipram treatment. Post-injury administration of rolipram increased atrophy and cavitation of the ipsilateral parietal cortex (A). Animals received vehicle (5% ethanol) or (±)-rolipram (3 mg/kg, i.v.) 30 min after moderate parasagittal FPI or sham surgery, then continuously until perfusion (subcutaneously via osmotic miniature pumps). Animals were perfused 10 days post-surgery. Shown are H&E and Luxol fast blue stained sections at bregma level −5.3 mm. Scale bars 500 μm. Contusion volumes (B) were significantly greater in (±)-rolipram-treated TBI animals as compared to vehicle-treated TBI animals at 10 days post-injury (***P < 0.001 for sham versus (±)-rolipram-treated TBI animals, #P < 0.01 for vehicle-treated versus (±)-rolipram-treated TBI animals). TBI-induced atrophy of the parietal cortex (C) was increased in (±)-rolipram-treated animals (**P < 0.01 and ***P < 0.001 for sham versus TBI animals, #P < 0.01 for vehicle-treated versus (±)-rolipram-treated TBI animals). Mean ± SEM, n = 3 vehicle-treated sham animals, n = 5 vehicle-treated TBI animals, n = 4 (±)-rolipram-treated TBI animals.