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The Journal of Neuroscience, April 7, 2004, 24(14):3543-3553; doi:10.1523/JNEUROSCI.5048-03.2004

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Neurobiology of Disease
Identification and Characterization of Heterogeneous Neuronal Injury and Death in Regions of Diffuse Brain Injury: Evidence for Multiple Independent Injury Phenotypes

Richard H. Singleton and John T. Povlishock

Department of Anatomy and Neurobiology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, Virginia 23298

Diffuse brain injury (DBI) is a consequence of traumatic brain injury evoked via rapid acceleration–deceleration of the cranium, giving rise to subtle pathological changes appreciated best at the microscopic level. DBI is believed to be comprised by diffuse axonal injury and other forms of diffuse vascular change. The potential, however, that the same forces can also directly injure neuronal somata in vivo has not been considered. Recently, while investigating DBI-mediated perisomatic axonal injury, we identified scattered, rapid neuronal somatic necrosis occurring within the same domains. Moving on the premise that these cells sustained direct somatic injury as a result of DBI, we initiated the current study, in which rats were intracerebroventricularly infused with various high-molecular weight tracers (HMWTs) to identify injury-induced neuronal somatic plasmalemmal disruption. These studies revealed that DBI caused immediate, scattered neuronal somatic plasmalemmal injury to all of the extracellular HMWTs used. Through this approach, a spectrum of neuronal change was observed, ranging from rapid necrosis of the tracer-laden neurons to little or no pathological change at the light and electron microscopic level. Parallel double and triple studies using markers of neuronal degeneration, stress, and axonal injury identified additional injured neuronal phenotypes arising in close proximity to, but independent of, neurons demonstrating plasmalemmal disruption. These findings reveal that direct neuronal somatic injury is a component of DBI, and diffuse trauma elicits a heretofore-unrecognized multifaceted neuronal pathological change within the CNS, generating heterogeneous injury and reactive alteration within both axons and neuronal somata in the same domains.

Key words: cortex; fluorescence; hippocampus; horseradish peroxidase; neuron; necrosis; traumatic brain injury; diffuse brain injury

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Received Nov 13, 2003; revised January 22, 2004; accepted February 17, 2004.

This article has been cited by other articles:

				P. Georgiadis, H. Xu, C. Chua, F. Hu, L. Collins, C. Huynh, E. F. LaGamma, and P. Ballabh Characterization of Acute Brain Injuries and Neurobehavioral Profiles in a Rabbit Model of Germinal Matrix Hemorrhage Stroke, December 1, 2008; 39(12): 3378 - 3388. [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]

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