TY - JOUR
T1 - Acute and late changes in N-acetyl-aspartate following diffuse axonal injury in rats
T2 - An MRI spectroscopy and microdialysis study
AU - Alessandri, B.
AU - Al-Samsam, R.
AU - Corwin, F.
AU - Fatouros, P.
AU - Young, H. F.
AU - Bullock, R. M.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2000
Y1 - 2000
N2 - N-acetyl-aspartate (NAA) measured by proton nuclear magnetic resonance spectroscopy (1H-NMR) has been used as a marker of neuronal injury in many cerebral pathologies. Therefore, we evaluate the roles of microdialysis vs. 1H-NMR as techniques to assess NAA (NAA)(d); NAA/Creatine ratio) in the living brain, and compare the results with whole brain NAA (NAA(w)), analyzed by HPLC after diffuse traumatic brain injury (TBI). Acute (4 h post-injury survival) and late (48 h survival) changes were studied in a sham-operated group (Sham, n = 4), and two injured groups (TBI/4 h, n = 8; TBI/48 h, n = 7). Baseline NAA(d) was 8.17±1 μM, and there was no significant difference between groups. There was only a small (twice of control), but transient increase in NAA(d) in the TBI/4 h group after trauma. Baseline NAA/Cr ratio was 1.35±0.2, which did not change significantly between baseline, 1, 2, 3, 4 and 48 h or between groups after TBI. Whole brain NAA(w) (baseline 8.5 ± 0.5 mmol kg-1 wet weight) did not differ significantly between groups before and after TBI. Diffuse TBI did not produce long-term changes in NAA, assessed by three different methods. These results may indicate that NAA is not a sensitive marker of the severity of diffuse axonal damage. However, further studies are needed to evaluate whether confounding factors such as microdialysis probe, voxel position and non-regional tissue homogenization might have influenced our data.
AB - N-acetyl-aspartate (NAA) measured by proton nuclear magnetic resonance spectroscopy (1H-NMR) has been used as a marker of neuronal injury in many cerebral pathologies. Therefore, we evaluate the roles of microdialysis vs. 1H-NMR as techniques to assess NAA (NAA)(d); NAA/Creatine ratio) in the living brain, and compare the results with whole brain NAA (NAA(w)), analyzed by HPLC after diffuse traumatic brain injury (TBI). Acute (4 h post-injury survival) and late (48 h survival) changes were studied in a sham-operated group (Sham, n = 4), and two injured groups (TBI/4 h, n = 8; TBI/48 h, n = 7). Baseline NAA(d) was 8.17±1 μM, and there was no significant difference between groups. There was only a small (twice of control), but transient increase in NAA(d) in the TBI/4 h group after trauma. Baseline NAA/Cr ratio was 1.35±0.2, which did not change significantly between baseline, 1, 2, 3, 4 and 48 h or between groups after TBI. Whole brain NAA(w) (baseline 8.5 ± 0.5 mmol kg-1 wet weight) did not differ significantly between groups before and after TBI. Diffuse TBI did not produce long-term changes in NAA, assessed by three different methods. These results may indicate that NAA is not a sensitive marker of the severity of diffuse axonal damage. However, further studies are needed to evaluate whether confounding factors such as microdialysis probe, voxel position and non-regional tissue homogenization might have influenced our data.
KW - Brain
KW - Halothane anesthesia
KW - Microdialysis
KW - N-acetyl-aspartate
KW - Neuronal death
KW - Proton nuclear magnetic resonance spectroscopy (H-NMR)
KW - Rat
KW - Traumatic brain injury
KW - Weight drop injury
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U2 - 10.1080/01616412.2000.11740744
DO - 10.1080/01616412.2000.11740744
M3 - Article
C2 - 11091977
AN - SCOPUS:0033746498
VL - 22
SP - 705
EP - 712
JO - Neurological Research
JF - Neurological Research
SN - 0161-6412
IS - 7
ER -