Figure 6

Neuroprotection at the brain tissue level by mAb1379 treatment of head-injured mice. Adjacent cryosections of 6–8 μm thickness are shown for sham-operated (panels A, D, H, K) and head-injured mice treated by placebo (panels B, E, I, L) or mAb 1379 (panels C, F, J, M) at the time-point of 7 days. Immunohistochemical staining by the use of a neuron-specific marker (NeuN, panels A-C) shows a significant tissue destruction of the cortical neuronal layers of the injured hemisphere in placebo-injected mice (B). In contrast, the injured hemisphere appears largely protected in mAb 1379-treated mice (C), showing a similarly intact neuronal cell layer morphology as in sham-operated animals (A). The staining of infiltrating leukocytes by a marker for complement receptor type 3 (CD11b, panels D-F) shows positive cells in the disrupted subarachnoid space of placebo-injected mice (E), but not in mAb 1379-injected animals (F). Furthermore, TUNEL-histochemistry (panels K-M) revealed positive cells in the injured hemisphere of placebo-injected head-injured mice (L), but not in mAb 1379-treated animals (M). The 4',6'-diamino-2-phenylindole (DAPI) stainings (panels H-J) show the overall nuclear morphology in adjacent sections to those stained by TUNEL. TBI, traumatic brain injury. Original magnifications: 100 ×.