Traumatically induced axotomy adjacent to the soma does not result in acute neuronal death.

摘要: Traumatic axonal injury (TAI), a consequence of traumatic brain (TBI), results from progressive pathologic processes initiated at the time injury. Studies attempting to characterize pathology associated with TAI have not succeeded in following damaged and/or disconnected segments back their individual neuronal somata determine fate. To address this issue, 71 adult male Sprague Dawley rats were subjected moderate central fluid percussion and killed between 30 min 7 d after Antibodies C terminus beta-amyloid precursor protein (APP) identified continuity mediodorsal neocortex, hilus dentate gyrus, dorsolateral thalamus. These followed immunocytochemical markers targeting phosphorylated 200 kDa neurofilaments (RMO-24), altered translation (phosphorylated eukaryotic initiation factor 2 alpha), cell death [terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)], parallel electron microscopic (EM) assessment. Despite finding within 20-50 micrometer soma, no evidence death, long proximal axotomy, was seen via TUNEL or routine light microscopy/electron microscopy. Rather, there rapid onset (<6 hr injury) subcellular change impaired synthesis by EM, immunocytochemical, Western blot analyses. When injury, these abnormalities did reveal dramatic progression. some showed potential reorganization repair. This study demonstrates novel somatic response perisomatic domain also provides insight into multifaceted TBI.