Abstract
BACKGROUND: Traumatic brain injury (TBI) is a complex condition and remains a prominent public and medical health issue in individuals of all ages. A rapid increase in extracellular glutamate occurs after TBI, leading to glutamate-induced excitotoxicity, which causes neuronal damage and further functional impairments. Although inhibition of glutamate carboxypeptidase II (GCP II) is considered a potential approach for reducing glutamate-induced excitotoxicity after TBI, further detailed evidence regarding its efficacy is required. Therefore, in this study, we examined the differences in the metabolite status between wild-type (WT) and GCP II gene-knockout (KO) mice after TBI using proton magnetic resonance spectroscopy (1H-MRS) and T2-weighted magnetic resonance (MR) imaging with a 7-tesla imaging system, and brain water-content analysis. RESULTS: Evaluation of glutamate and N-acetylaspartate concentrations revealed a decrease in both levels in the ipsilateral hippocampus at 24 h post-TBI; however, the reduction in glutamate and N-acetylaspartate levels was less marked in GCP II-KO mice than in WT mice (p < 0.05). T2 MR data and brain water-content analysis demonstrated that the extent of cortical edema and brain swelling was less in KO than in WT mice after TBI (p < 0.05). CONCLUSION: Using two non-invasive methods, 1H-MRS and T2 MR imaging, as well as in vitro brain-water content measurements, we demonstrated that the mechanism underlying the neuroprotective effects of GCP II-KO against brain swelling in TBI involves changes in glutamate and N-acetylaspartate levels. This knowledge may contribute towards the development of therapeutic strategies for TBI.
| Original language | English (US) |
|---|---|
| Number of pages | 1 |
| Journal | BMC Neuroscience |
| Volume | 19 |
| Issue number | 1 |
| DOIs | |
| State | Published - Nov 20 2018 |
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Keywords
- Brain edema
- Glutamate
- Glutamate carboxypeptidase II
- Proton magnetic resonance spectroscopy (1H-MRS)
- Traumatic brain injury
ASJC Scopus subject areas
- Neuroscience(all)
- Cellular and Molecular Neuroscience
Cite this
Metabolite differences between glutamate carboxypeptidase II gene knockout mice and their wild-type littermates after traumatic brain injury : a 7-tesla 1H-MRS study. / Wu, Wenbo; Xu, Siyi; Wang, Jialin; Zhang, Kuiming; Zhang, Mingkun; Cao, Yang; Ren, Hongqing; Zheng, Deyou; Zhong, Chunlong.
In: BMC Neuroscience, Vol. 19, No. 1, 20.11.2018.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Metabolite differences between glutamate carboxypeptidase II gene knockout mice and their wild-type littermates after traumatic brain injury
T2 - a 7-tesla 1H-MRS study
AU - Wu, Wenbo
AU - Xu, Siyi
AU - Wang, Jialin
AU - Zhang, Kuiming
AU - Zhang, Mingkun
AU - Cao, Yang
AU - Ren, Hongqing
AU - Zheng, Deyou
AU - Zhong, Chunlong
PY - 2018/11/20
Y1 - 2018/11/20
N2 - BACKGROUND: Traumatic brain injury (TBI) is a complex condition and remains a prominent public and medical health issue in individuals of all ages. A rapid increase in extracellular glutamate occurs after TBI, leading to glutamate-induced excitotoxicity, which causes neuronal damage and further functional impairments. Although inhibition of glutamate carboxypeptidase II (GCP II) is considered a potential approach for reducing glutamate-induced excitotoxicity after TBI, further detailed evidence regarding its efficacy is required. Therefore, in this study, we examined the differences in the metabolite status between wild-type (WT) and GCP II gene-knockout (KO) mice after TBI using proton magnetic resonance spectroscopy (1H-MRS) and T2-weighted magnetic resonance (MR) imaging with a 7-tesla imaging system, and brain water-content analysis. RESULTS: Evaluation of glutamate and N-acetylaspartate concentrations revealed a decrease in both levels in the ipsilateral hippocampus at 24 h post-TBI; however, the reduction in glutamate and N-acetylaspartate levels was less marked in GCP II-KO mice than in WT mice (p < 0.05). T2 MR data and brain water-content analysis demonstrated that the extent of cortical edema and brain swelling was less in KO than in WT mice after TBI (p < 0.05). CONCLUSION: Using two non-invasive methods, 1H-MRS and T2 MR imaging, as well as in vitro brain-water content measurements, we demonstrated that the mechanism underlying the neuroprotective effects of GCP II-KO against brain swelling in TBI involves changes in glutamate and N-acetylaspartate levels. This knowledge may contribute towards the development of therapeutic strategies for TBI.
AB - BACKGROUND: Traumatic brain injury (TBI) is a complex condition and remains a prominent public and medical health issue in individuals of all ages. A rapid increase in extracellular glutamate occurs after TBI, leading to glutamate-induced excitotoxicity, which causes neuronal damage and further functional impairments. Although inhibition of glutamate carboxypeptidase II (GCP II) is considered a potential approach for reducing glutamate-induced excitotoxicity after TBI, further detailed evidence regarding its efficacy is required. Therefore, in this study, we examined the differences in the metabolite status between wild-type (WT) and GCP II gene-knockout (KO) mice after TBI using proton magnetic resonance spectroscopy (1H-MRS) and T2-weighted magnetic resonance (MR) imaging with a 7-tesla imaging system, and brain water-content analysis. RESULTS: Evaluation of glutamate and N-acetylaspartate concentrations revealed a decrease in both levels in the ipsilateral hippocampus at 24 h post-TBI; however, the reduction in glutamate and N-acetylaspartate levels was less marked in GCP II-KO mice than in WT mice (p < 0.05). T2 MR data and brain water-content analysis demonstrated that the extent of cortical edema and brain swelling was less in KO than in WT mice after TBI (p < 0.05). CONCLUSION: Using two non-invasive methods, 1H-MRS and T2 MR imaging, as well as in vitro brain-water content measurements, we demonstrated that the mechanism underlying the neuroprotective effects of GCP II-KO against brain swelling in TBI involves changes in glutamate and N-acetylaspartate levels. This knowledge may contribute towards the development of therapeutic strategies for TBI.
KW - Brain edema
KW - Glutamate
KW - Glutamate carboxypeptidase II
KW - Proton magnetic resonance spectroscopy (1H-MRS)
KW - Traumatic brain injury
UR - http://www.scopus.com/inward/record.url?scp=85056802283&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85056802283&partnerID=8YFLogxK
U2 - 10.1186/s12868-018-0473-5
DO - 10.1186/s12868-018-0473-5
M3 - Article
VL - 19
JO - BMC Neuroscience
JF - BMC Neuroscience
SN - 1471-2202
IS - 1
ER -