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Neural Plasticity
Volume 2016 (2016), Article ID 1347987, 10 pages
Research Article

Astrocyte Hypertrophy Contributes to Aberrant Neurogenesis after Traumatic Brain Injury

1Department of Surgery, Texas A&M University Health Science Center, College of Medicine, Temple, TX 76504, USA
2Central Texas Veterans Health Care System, Temple, TX 76504, USA
3Department of Neurosurgery, Neuroscience Research Institute, Scott & White Hospital, Temple, TX 76508, USA

Received 10 November 2015; Accepted 11 February 2016

Academic Editor: Fushun Wang

Copyright © 2016 Clark Robinson et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Traumatic brain injury (TBI) is a widespread epidemic with severe cognitive, affective, and behavioral consequences. TBIs typically result in a relatively rapid inflammatory and neuroinflammatory response. A major component of the neuroinflammatory response is astrocytes, a type of glial cell in the brain. Astrocytes are important in maintaining the integrity of neuronal functioning, and it is possible that astrocyte hypertrophy after TBIs might contribute to pathogenesis. The hippocampus is a unique brain region, because neurogenesis persists in adults. Accumulating evidence supports the functional importance of these newborn neurons and their associated astrocytes. Alterations to either of these cell types can influence neuronal functioning. To determine if hypertrophied astrocytes might negatively influence immature neurons in the dentate gyrus, astrocyte and newborn neurons were analyzed at 30 days following a TBI in mice. The results demonstrate a loss of radial glial-like processes extending through the granule cell layer after TBI, as well as ectopic growth and migration of immature dentate neurons. The results further show newborn neurons in close association with hypertrophied astrocytes, suggesting a role for the astrocytes in aberrant neurogenesis. Future studies are needed to determine the functional significance of these alterations to the astrocyte/immature neurons after TBI.