Traumatic brain injury and hippocampal neurogenesis: Functional implications

In the adult brain, self-renewing radial-glia like (RGL) progenitor cells have been shown to reside in the subventricular zone and the subgranular zone of the hippocampus. A large body of evidence shows that experiences such as learning, enriched environment and stress can alter proliferation and di...

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Bibliographic Details
Published in:Experimental neurology 2020-09, Vol.331, p.113372-113372, Article 113372
Main Authors: Redell, John B., Maynard, Mark E., Underwood, Erica L., Vita, Sydney M., Dash, Pramod K., Kobori, Nobuhide
Format: Article
Language:English
Subjects:
Animals
Brain Injuries, Traumatic - pathology
Brain Injuries, Traumatic - physiopathology
Context discrimination
Hippocampus
Hippocampus - pathology
Hippocampus - physiopathology
Humans
Neurogenesis - physiology
Pattern separation
Subgranular zone
Traumatic brain injury
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Summary:In the adult brain, self-renewing radial-glia like (RGL) progenitor cells have been shown to reside in the subventricular zone and the subgranular zone of the hippocampus. A large body of evidence shows that experiences such as learning, enriched environment and stress can alter proliferation and differentiation of RGL progenitor cells. The progenitor cells present in the subgranular zone of the hippocampus divide to give rise to newborn neurons that migrate to the dentate gyrus where they differentiate into adult granule neurons. These newborn neurons have been found to have a unique role in certain types of hippocampus-dependent learning and memory, including goal-directed behaviors that require pattern separation. Experimental traumatic brain injury (TBI) in rodents has been shown to alter hippocampal neurogenesis, including triggering the acute loss of newborn neurons, as well as progenitor cell hyper-proliferation. In this review, we discuss the role of hippocampal neurogenesis in learning and memory. Furthermore, we review evidence for the molecular mechanisms that contribute to newborn neuron loss, as well as increased progenitor cell proliferation after TBI. Finally, we discuss strategies aimed at enhancing neurogenesis after TBI and their possible therapeutic benefits.
ISSN:0014-4886
1090-2430
DOI:10.1016/j.expneurol.2020.113372