Decrease and recovery of N-acetylaspartate/creatine in rat brain remote from focal injury.

Abstract

Magnetic resonance spectroscopy (MRS) studies on traumatic brain injury (TBI) have shown that the neuronal metabolite N-acetylaspartate (NAA) may be reduced in regions of brain remote from sites of focal injury. Such reductions have generally been attributed to diffuse axonal injury (DAI) or neuron death. The aim of the present study was to investigate the contribution of metabolic depression, in the absence of DAI or cell death, to remote NAA reduction after TBI. The right sensorimotor cortices of adult rats were injured by weight drop. Two and six days later, tissue slices from the ipsilateral occipital cortex, or from the same region in uninjured rats, were superfused and examined by 1H-MRS. The occipital cortex has been shown to have negligible DAI or cell death but marked transient metabolic depression in this model of TBI. Two days after injury, the ratio of the NAA peak height to the total creatine peak height (NAA/TCr) was 14% lower than in control samples. Six days after injury, NAA/TCr recovered to within 7% of the control value. The time course of NAA/TCr decrease and recovery was similar to the time courses of widespread depression and recovery of 2-deoxyglucose uptake and mitochondrial alpha-glycerophosphate dehydrogenase activity measured previously in this model of TBI. Together, these results suggest that at least one component of remote NAA depression after TBI may be associated with a widespread and reversible metabolic depression that is unrelated to either DAI or cell death.