Moderate traumatic brain injury causes acute dendritic and synaptic degeneration in the hippocampal dentate gyrus
Open accessAbstract
Hippocampal injury-associated learning and memory deficits are frequent hallmarks of brain trauma and are the most enduring and devastating consequences following traumatic brain injury (TBI). Several reports, including our recent paper, showed that TBI brought on by a moderate level of controlled cortical impact (CCI) induces immature newborn neuron death in the hippocampal dentate gyrus. In contrast, the majority of mature neurons are spared. Less research has been focused on these spared neurons, which may also be injured or compromised by TBI. Here we examined the dendrite morphologies, dendritic spines, and synaptic structures using a genetic approach in combination with immunohistochemistry and Golgi staining. We found that although most of the mature granular neurons were spared following TBI at a moderate level of impact, they exhibited dramatic dendritic beading and fragmentation, decreased number of dendritic branches, and a lower density of dendritic spines, particularly the mushroom-shaped mature spines. Further studies showed that the density of synapses in the molecular layer of the hippocampal dentate gyrus was significantly reduced. The electrophysiological activity of neurons was impaired as well. These results indicate that TBI not only induces cell death in immature granular neurons, it also causes significant dendritic and synaptic degeneration in pathohistology. TBI also impairs the function of the spared mature granular neurons in the hippocampal dentate gyrus. These observations point to a potential anatomic substrate to explain, in part, the development of posttraumatic memory deficits. They also indicate that dendritic damage in the hippocampal dentate gyrus may serve as a therapeutic target following TBI.
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Dendritic swelling and beading are hallmarks of dendritic injury.
“dendritic swelling and beading, both of which are hallmarks of dendritic injury [38]”
From Hippocampal neuro-networks and dendritic spine perturbations in epileptogenesis are attenuated by neuroprotectin D1 (2015) · cites this paper as [38]
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Molecular mechanisms of cognitive dysfunction following traumatic brain injury
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- Authors
- Gao, X., Deng, P., Xu, Z. C., & Chen, J.
- Affiliations
- Indiana University Indianapolis (US)
- Corresponding author
- Chen, Jinhui
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2011-09-13
- Volume
- 6
- Issue
- 9
- Pages
- e24566
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3172233
- OpenAlex
- W1964169664
- Cited by
- 218
- References
- 76
- Citations by year
- 2026: 10 · 2025: 9 · 2024: 13 · 2023: 10 · 2022: 19 · 2021: 20 · 2020: 20 · 2019: 19 · 2018: 15 · 2017: 20 · 2016: 22 · 2015: 17 · 2014: 9 · 2013: 12 · 2012: 3
- FWCI
- 4.86
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- IUScholarWorks (Indiana University) (submittedVersion, cc-by)
- Funders
- Smithsonian Conservation Biology Institute
- National Institute of Neurological Disorders and Stroke (R21NS072631, R21NS075733)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- traumatic brain injury, dentate gyrus, dendritic degeneration, dendritic spines, synaptic degeneration, controlled cortical impact, synaptic density
- MeSH terms
- Animals, Brain Injuries, Golgi Apparatus, Hippocampus, Male, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Fluorescence, Neurons, Perfusion, Synapses, Time Factors, Dentate Gyrus, Neurodegenerative Diseases, Green Fluorescent Proteins, Mice
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