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The Journal of Neuroscience, February 1, 2002, 22(3):791-802

Traumatically Induced Axotomy Adjacent to the Soma Does Not Result in Acute Neuronal Death

Richard H. Singleton¹, Jiepei Zhu², James R. Stone³, and John T. Povlishock¹

Departments of ¹ Anatomy and ²  Anesthesiology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, Virginia 23298, and ³ Department of Neurological Surgery, University of Virginia, Charlottesville, Virginia 22904

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

Key words: traumatic brain injury; traumatic axonal injury; axotomy; axon reaction; rat; protein translation; TUNEL

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Copyright © 2002 Society for Neuroscience  0270-6474/02/223791-12$05.00/0

This article has been cited by other articles:

				B.A. Cohen, M. Inglese, H. Rusinek, J.S. Babb, R.I. Grossman, and O. Gonen Proton MR Spectroscopy and MRI-Volumetry in Mild Traumatic Brain Injury AJNR Am. J. Neuroradiol., May 1, 2007; 28(5): 907 - 913. [Abstract] [Full Text] [PDF]

				O. Farkas, J. Lifshitz, and J. T. Povlishock Mechanoporation induced by diffuse traumatic brain injury: an irreversible or reversible response to injury? J. Neurosci., March 22, 2006; 26(12): 3130 - 3140. [Abstract] [Full Text] [PDF]

				R. H. Singleton and J. T. Povlishock Identification and Characterization of Heterogeneous Neuronal Injury and Death in Regions of Diffuse Brain Injury: Evidence for Multiple Independent Injury Phenotypes J. Neurosci., April 7, 2004; 24(14): 3543 - 3553. [Abstract] [Full Text] [PDF]

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