Conversion of brain cytosol profile from fetal to adult type during the perinatal period: Taurine-NAA exchange

Mammals face drastic environmental changes at birth. Appropriate adjustments of various systems must take place rapidly to accommodate this once in a life time event. The brain undergoes significant adjustments as well, the most obvious of which is in its need to meet the drastic increase in energy consumption at the neuronal cell membrane due to the explosive increase in neural activities after birth. Actual changes were found to be taken place in two systems, namely, acid base balance control and cytosolic energy transport. The adjustments are accomplished by converting cytosol microenvironment from a taurine rich fetal type environment to an N-acetyl-aspartate (NAA) rich adult type environment during the post-natal period. High concentrations of taurine are necessary to provide effective buffering in the fetal brain, because the fetus cannot utilize the adult type of pCO2 dependent acid–base balance control system, namely respiration driven pCO2 changes. To accommodate the significantly higher demand of energy consumption at the membrane due to the increased neuronal activities, taurine has to be replaced by NAA, since the latter facilitates HEP transport from mitochondria to the membrane by passive diffusion

Early and Sustained Alterations in Cerebral Metabolism after Traumatic Brain Injury in Immature Rats

Although studies have shown alterations in cerebral metabolism after traumatic brain injury (TBI), clinical data in the developing brain is limited. We hypothesized that post-traumatic metabolic changes occur early (<24 h) and persist for up to 1 week. Immature rats underwent TBI to the left parietal cortex. Brains were removed at 4 h, 24 h, and 7 days after injury, and separated into ipsilateral (injured) and contralateral (control) hemispheres. Proton nuclear magnetic resonance (NMR) spectra were obtained, and spectra were analyzed for N-acetyl-aspartate (NAA), lactate (Lac), creatine (Cr), choline, and alanine, with metabolite ratios determined (NAA/Cr, Lac/Cr). There were no metabolic differences at any time in sham controls between cerebral hemispheres. At 4 and 24 h, there was an increase in Lac/Cr, reflecting increased glycolysis and/or decreased oxidative metabolism. At 24 h and 7 days, there was a decrease in NAA/Cr, indicating loss of neuronal integrity. The NAA/Lac ratio was decreased (∼15–20%) at all times (4 h, 24 h, 7 days) in the injured hemisphere of TBI rats. In conclusion, metabolic derangements begin early (<24 h) after TBI in the immature rat and are sustained for up to 7 days. Evaluation of early metabolic alterations after TBI could identify novel targets for neuroprotection in the developing brain