Traumatic brain injury in mice deficient in Bid: effects on histopathology and functional outcome

Bid is a proapoptotic member of the Bcl-2 family that mediates cell death by caspase-dependent and -independent pathways. We tested mice genetically deficient in Bid in a controlled cortical impact (CCI) model to examine the hypothesis that Bid contributes to cell death and functional outcome after traumatic brain injury. After CCI, truncated Bid (15 kDa) was robustly detected in cortical brain homogenates of wild-type mice. Bid/ mice had decreased numbers of cortical cells with acute plasmalemma injury at 6 h (wild type (WT), 17216124; Bid/, 11736129 cells/ 200 field; P < 0.01), decreased numbers of cells expressing cleaved caspase-3 in the dentate gyrus at 48 h (WT, 113615; Bid/ ,6 569 cells/ 200 field; P < 0.05), and reduced lesion volume at 12 days (Bid/, 5.96 0.4 mm 3 ; WT, 8.460.4 mm 3 ; P < 0.001), but did not differ from WT mice at later times after injury