Abstract
The current difficulty of predicting the progression of cerebral degeneration and recovery after head injury hampers making appropriate treatment. The lack of clinically relevant animal model is the most significant problem in the basic research of head injury. Even mechanical impact without skull fracture leads to contusion in human brain, however this process is hardly mimicked in rodents. Thus, classical head-injury models have been created by giving impact to brain parenchyma through craniotomy. Most models show long-term degeneration and lack recovery, largely due to craniotomy, which activates glial cells by itself. In order to address this problem, we have developed a novel method to create injury by strong light exposure through small thinned-skull region. This intact skull injury have shown hemorrhage within 24 hours and significant shrinkage of initial injured region to form small contusion. This cerebral recovery has been accompanied by the accumulation of CD68-positive microglia and nestin-positive astrocyte in the center and periphery of lesion, respectively. The process of nestin-positive reactive astrocyte covered recovering region, whereas reactive astrocyte distal to lesion lacked nestin expression. Since fatty acid has accumulated in the nestin-expressing reactive astrocytes, these cells may facilitate tissue recovery by maintaining energy metabolism in lesion.
