Biology Reference
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(A)
(B)
(C)
(D)
(E)
(F)
Figure 10.1
Representative microscope images of the injured hemisphere following
experimental focal closed head injury in the mouse. Immunohistochemistry against neurons
(NeuN) (A, D), astrocytes (GFAP) (B, E), and macrophage/microglia (F4/80) (C, F) on
brain sections detected neuronal loss, astrocyte activation, and macrophage accumulation,
respectively. Note that by 7 days postinjury (A, B, C), F4/80-labeled macrophages are closely
compacted into the lesion core, which is devoid of viable neurons or astrocytes. By 28 days
postinjury (D, E, F), tissue damage is evident distally from the cortical lesion; increased
astrocyte (E) and microglial reactivity (F) in the dorsolateral thalamus corresponds to reduced
neuronal density in this region. Scale bar 1,000 m.
processes, whereas astrocytes seem to play a more protective role. However, benefi-
cial removal of dead cells by activated microglia/macrophages is crucial for tissue
repair, as it sequesters proteins that would otherwise perpetuate the inflammatory
response and myelin components that are known to detrimentally affect regeneration.
Activated astrocytes support repair mechanisms by releasing neurotrophic factors that
sustain neuronal survival as well as proliferation and differentiation of neural progen-
itor cells, thus promoting neurogenesis. In contrast, the glial scar has been implicated
in hampering neuronal and axonal regeneration, likely by the expression of inhibitory
proteins. Like the activation of microglia/macrophages, astrocyte reactivity is a long-
lasting process observed after both human and rodent TBI.
Although moderately present in the area surrounding a focal contusion, axonal
damage is mostly predominant in human or animal models of diffuse brain trauma.
The acceleration-deceleration impact injury model established by Marmarou et al.
