Effects of activated microglia and spreading depression on the injured CNS tissue

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Our modified fluid-percussion injury device was restored to make reproducible traumatic brain injuries in rats. Microglial activation and neuronal cell loss in the thalamus was well reproduced in this modelMildly injured animals without macroscopic brain loss had minimal motor disturbance, which was only noted in the beam-balancing task. However, memory disturbance was clearly demonstrated.At 1 hour following injury, resting microglia were activated to show morphological changes. "Bushy type" microglia increased all over the bilateral hippocampus. "Amoeboid type" microglia were noted in the ipsilateral CA1, CA4 and bilateral dentate gyrus. "Rod type" microglia were often found along the dendrites of HRP incorporated neurons. At 6 hours, "bushy type" microglia were returned to the resting type. However, "amoeboid type" microglia were still remained in the site.In the subacute stage (1 to 7 days) of traumatic brain injury, reactions of microglia and astrocyte, and axonal injuries were studied. Axonal injuries in the thalamus were seemed to be closely associated with the activated microglia.The number of survived neuronal cells in the single FK506 treated rats was significantly larger than the vehicle treated rats at 7 and 14 days following injury. However, the number in daily FK506 treated rats did not differ from that in the vehicle treated rats. The number of OX42 positive microglia in daily FK506 treated rats was significantly fewer than that in vehicle treated rats. FK506, when administered immediately after the injury, appeared to limit neuronal cell death in LD nucleus in traumatic brain injury in ratsSpreading depression studies were started using controlled cortical impact injury model.