Article
Neurocognitive and neuropathological changes in the hippocampus after traumatic brain injury in a rat model
Neurokognitive und neuropathologische Veränderungen im Hippocampus nach experimentellem Schädel-Hirntrauma im Rattenmodell
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Authors
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Martin Grutza
- Universitätsklinikum Heidelberg, Neurochirurgische Klinik, Heidelberg, Deutschland
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Karin Große
- Universitätsklinikum Heidelberg, Neurochirurgische Klinik, Heidelberg, Deutschland
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Andreas W. Unterberg
- Universitätsklinikum Heidelberg, Neurochirurgische Klinik, Heidelberg, Deutschland
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Klaus Zweckberger
- Universitätsklinikum Heidelberg, Neurochirurgische Klinik, Heidelberg, Deutschland
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Alexander Younsi
- Universitätsklinikum Heidelberg, Neurochirurgische Klinik, Heidelberg, Deutschland
| Published: | May 25, 2022 |
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Outline
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Objective: Traumatic Brain Injury (TBI) is a progressive and complex pathological condition which is frequently associated with impairment of cognitive function, including learning and memory. Such deficits are thought to be related with damage of the hippocampus. However, little is known about long-term neurocognitive and histopathological changes after hippocampal injury. Thus, we aimed to study such long-term effects in an experimental hippocampal TBI model in rats.
Methods: Male Wistar rats were subjected to either right parietal Controlled Cortical Impact (CCI) with a depth of 3 mm, a contact time of 150 ms and an impact speed of 8 m/sec or sham surgery. Motor function was examined via the Rotarod (RR) test 24 h, 72 h, 7 days, 14 days, and 28 days after injury. Learning and memory function were tested via the Sacktor’s Active Avoidance test (AAT) 4 days, 12 days and 24 days after CCI. Hippocampal atrophy and neuronal loss were histologically examined with Nissl-Staining. Results were compared between both groups and correlation analyses were performed.
Results: In comparison to uninjured sham animals, motor deficits were significantly increased in the RR 24 h and 72 h after CCI. A slight recovery of injured animals was observed at day 7 and reached a plateau at day 14. Moreover, CCI resulted in significant deficits in spatial learning and memory in the AAT which slightly improved again after 14 days. In comparison, sham animals showed improvement 4 days, 12 days, and 24 days after surgery. Nissl-Staining demonstrated severe neuronal loss and atrophy in the hippocampus after 14 days which further worsened until day 28 after CCI. Spearman correlation analyses showed significant associations between neuronal loss in the hippocampus and deficits in spatial learning and memory in the Sacktor’s Active Avoidance test.
Conclusion: Our study gives a better understanding of not only the short -but also the long-term histopathological changes in the hippocampus and neurobehavior changes after experimentally induced TBI. These results might allow for refined evaluation of experimental therapeutic methods in future preclinical animal experiments.
