['To establish the molecular background for glucocorticoid insensitivity, that is, failure to reduce edema formation and to protect blood-brain barrier integrity after acute traumatic brain injury.', 'Controlled animal study.', 'University research laboratory.', 'Male C57Bl/6N mice.', 'Mechanical brain lesion by controlled cortical impact.', 'Our study demonstrates that 1) proteasomal glucocorticoid receptor degradation is established in brain endothelial cells after traumatic brain injury as a form of posttranslational glucocorticoid receptor modification; 2) inhibition of the proteasomal degradation pathway with bortezomib (0.2 mg/kg) in combination with the glucocorticoid dexamethasone (10 mg/kg) by subcutaneous injection 30 minutes postinjury restores levels of barrier sealing glucocorticoid receptor target occludin in brain endothelial cells, improves blood-brain barrier integrity, reduces edema formation, and limits neuronal damage after brain trauma.'] Does inhibition of proteasomal glucocorticoid receptor degradation restore dexamethasone-mediated stabilization of the blood-brain barrier after traumatic brain injury?