Acute and late changes in N-acetyl-aspartate following diffuse axonal injury in rats: An MRI spectroscopy and microdialysis study

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.