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Updated: Jul 10, 2026

Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Posttraumatic secondary brain insults exacerbates neuronal injury by altering metabotropic glutamate receptors
Zhou Fei1, Xiang Zhang, Hong-Min Bai
1Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, PR China. feizhou@fmmu.edu.cn
Background:
Our previous studies indicated that metabotropic glutamate receptors (mGluRs) are deeply involved in the secondary processes after diffuse brain injury (DBI). In the present study, we used a rodent DBI model to determine whether hypotension exacerbates neuronal injury as a secondary brain insult (SBI) after traumatic brain injury (TBI) by changing the expression of metabotropic glutamate receptors (mGluRs) in the cerebral cortex.
Results:
Three hundred and eleven male Sprague-Dawley rats were randomly assigned into five groups: normal control, sham-operated control, SBI alone, DBI alone, or DBI with SBI. DBI was produced in rats by Marmarou's methods and the SBI model was produced by hypotension. The alteration of neuronal expression of mGluRs after DBI and DBI coupled with SBI was observed by hybridization in situ at different time points in the experiment. We found a higher mortality and neurological severity score (NSS) for rats in the DBI with SBI group compared with those in the DBI alone group. Although there was a significant rise in the expression of group I and group III mGluRs (except mGluR6) and a decrease in the expression of group II mGluRs after DBI (P < 0.05), the changes were more severe when DBI was coupled with SBI (P < 0.05). The expression of group I mGluRs peaked at 24 hours, while the expression of the group III mGluRs peaked at 6 hours after injuries, which may reflect a self-protection first mechanism of the damaged neurons. Moreover, the overall neuro-harmful effects of mGluRs on neurons were seemly associated with higher mortality and NSS in the DBI with SBI group.
Conclusion:
The results suggest posttraumatic SBI may exacerbate neuronal injury or brain injury by altering expression of mGluRs, and more emphasis should therefore be put on the prevention and treatment of SBI.
Insights
Hypotension following traumatic brain injury (TBI) worsens neuronal damage by altering metabotropic glutamate receptors (mGluRs). Preventing secondary brain insults (SBI) is crucial for better outcomes after TBI.
Area of Science:
- Neuroscience
- Neurotrauma
- Molecular Biology
Background:
- Metabotropic glutamate receptors (mGluRs) are implicated in secondary processes following diffuse brain injury (DBI).
- Previous research suggests mGluRs play a role in brain injury secondary insults.
Purpose of the Study:
- To investigate if hypotension exacerbates neuronal injury after traumatic brain injury (TBI).
- To determine if secondary brain insults (SBI) alter metabotropic glutamate receptor (mGluR) expression in the cerebral cortex following DBI.
Main Methods:
- A rodent model of diffuse brain injury (DBI) and secondary brain insult (SBI) induced by hypotension was utilized.
- Neuronal expression of mGluRs was analyzed using in situ hybridization at various time points post-injury.
- Mortality and neurological severity scores (NSS) were assessed across different experimental groups.
Main Results:
- DBI combined with SBI resulted in higher mortality and neurological severity scores (NSS) compared to DBI alone.
- DBI altered mGluR expression, with increased Group I and III mGluRs and decreased Group II mGluRs.
- These mGluR expression changes were more pronounced in the DBI with SBI group, correlating with increased neuro-harmful effects.
Conclusions:
- Secondary brain insults (SBI), such as hypotension, exacerbate neuronal injury after TBI by altering mGluR expression.
- Preventing and treating SBI is critical to mitigate secondary brain injury and improve patient outcomes.
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