Histological markers of neuronal, axonal and astrocytic changes after lateral rigid impact traumatic brain injury.
The model of lateral, rigid impact traumatic brain injury is widely used but remains relatively poorly characterized by comparison with fluid percussion injury models. Thus, whilst the gross morphological changes that occur over the short- and long-term post-injury have been described, more subtle measures of neuronal injury and activation, and markers of axonal and glial reactions have not been investigated, complicating interpretation of data from this model. To address this issue, a variety of neurohistological markers were examined in adult male rats which had been subjected to open brain, lateral rigid impact injury. A piston device was unilaterally driven 3.0 mm into the somatosensory cortex at a speed of 3.2 m/s. Neuronal activation evidenced by Fos-like immunoreactivity showed a complex pattern at 3 h after injury which appeared to be related both to proximity to the impact site and cortical efferent connectivity. At 24 h after injury, acid fuchsin staining demonstrated dying neurons in the margin of the injury and in ipsilateral hippocampus and dorsal thalamus. Injured cells identified by heat-shock protein immunoreactivity showed a similar distribution. Axonal injury demonstrated with 68 kDa neurofilament immunoreactivity was more widely distributed. Less axonal damage was found with increasing distance from the injury site. At 7 days post-injury, glial fibrillary acidic protein immunoreactive astrocytes were prolific in the ipsilateral thalamus, hippocampus and striatum and throughout the injured cortex. In general, controlled, lateral rigid impact injury provides a more focused injury than is seen with lateral fluid percussion which may have implications for the behavioral deficits seen in this injury model.
Dunn-Meynell
A A
AA
Neurology Service, Department of Veterans Affairs Medical Center, East Orange, NJ 07018-1095, USA.
Levin
B E
BE
D000818:Animals; D001253:Astrocytes / Q000737:chemistry* / Q000166:cytology; D001369:Axons / Q000737:chemistry*; D001557:Benzenesulfonates; D048588:Benzoxazines; D015415:Biomarkers; D001930:Brain Injuries / Q000378:metabolism*; D004396:Coloring Agents; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000032:analysis; D007150:Immunohistochemistry; D008297:Male; D009410:Nerve Degeneration / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000032:analysis; D016900:Neurofilament Proteins / Q000032:analysis; D009474:Neurons / Q000737:chemistry* / Q000166:cytology / Q000648:ultrastructure; D010078:Oxazines; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D001557:Benzenesulfonates; D048588:Benzoxazines; D015415:Biomarkers; D004396:Coloring Agents; D005904:Glial Fibrillary Acidic Protein; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D009419:Nerve Tissue Proteins; D016900:Neurofilament Proteins; D010078:Oxazines; D016760:Proto-Oncogene Proteins c-fos; C066858:neurofilament protein NF 68; C028911:cresyl violet; C086337:acid fuchsin