2. Cell Proliferation in the Brains of Adult Rats Exposed to Traumatic Brain Injury

  1. Peter R. Mouton PhD
  1. Sandra A. Acosta1,
  2. Naoki Tajiri1,
  3. Paula C. Bickford2 and
  4. Cesar V. Borlongan1

Published Online: 22 NOV 2013

DOI: 10.1002/9781118444177.ch2

Neurostereology: Unbiased Stereology of Neural Systems

Neurostereology: Unbiased Stereology of Neural Systems

How to Cite

Acosta, S. A., Tajiri, N., Bickford, P. C. and Borlongan, C. V. (2014) Cell Proliferation in the Brains of Adult Rats Exposed to Traumatic Brain Injury, in Neurostereology: Unbiased Stereology of Neural Systems (ed P. R. Mouton), John Wiley & Sons, Inc., Ames, USA. doi: 10.1002/9781118444177.ch2

Author Information

  1. 1

    Center of Excellence for Aging and Brain Repair, Department of Neurosurgery and Brain Repair, University of South Florida College of Medicine, Tampa, FL, USA

  2. 2

    James A. Haley Veterans Affairs Hospital, Tampa, FL, USA

Publication History

  1. Published Online: 22 NOV 2013
  2. Published Print: 17 JAN 2014

ISBN Information

Print ISBN: 9781118444214

Online ISBN: 9781118444177

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Keywords:

  • adult rats;
  • brain;
  • cell proliferation;
  • gray matter;
  • traumatic brain injury (TBI)

Summary

This chapter presents a study in which the authors used an in vivo model of chronic traumatic brain injury (TBI) to examine the neuroinflammatory responses in subcortical regions of gray matter (dorsal striatum, thalamus) and white matter (corpus callosum, hippocampal fimbria-fornix, and cerebral peduncle). The authors evaluated neuronal cell loss, cell proliferation, and neuronal differentiation in neurogenic niches in order to assess progressive secondary injuries in these vital regenerative brain areas. The overall findings support the concept that massive neuroinflammation following TBI leads to a second wave of cell death, creating a chronic TBI condition that impairs the proliferative capacity of cells and impedes neurogenesis. The study suggests that chronic TBI causes cell proliferation through a cascade of events. The findings suggest that while TBI is considered an acute injury, the disease pathology over the long term includes both a chronic cell death perturbation and a diminished endogenous repair mechanism.