Upregulation of ICAM-1 and MCP-1 but not of MIP-2 and sensorimotor deficit in response to traumatic axonal injury in rats.

@article{Rancan2001UpregulationOI,
  title={Upregulation of ICAM-1 and MCP-1 but not of MIP-2 and sensorimotor deficit in response to traumatic axonal injury in rats.},
  author={Mario Rancan and Vivianne I. Otto and Volkmar H. Hans and Irene Gerlach and Reinhard Jork and Otmar L Trentz and Thomas Kossmann and Maria Cristina Morganti-Kossmann},
  journal={Journal of neuroscience research},
  year={2001},
  volume={63 5},
  pages={438-46}
}
The pathophysiology of traumatic axonal injury (TAI) is only partially understood. In this study, we investigated the inflammatory response as well as the extent of neurological deficit in a rat model of traumatic brain injury (TBI). Forty-two adult rats were subjected to moderate impact-acceleration brain injury and their brains were analyzed immunohistochemically for ICAM-1 expression and neutrophil infiltration from 1 hr up to 14 days after trauma. In addition, the chemotactic factors MIP-2… CONTINUE READING

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