Cerebral glucose metabolism in an immature rat model of pediatric traumatic brain injury

Courtney L. Robertson, Manda Saraswati, Susanna Scafidi, Gary Fiskum, Paula Casey, Mary C. McKenna

Research output: Contribution to journalArticle

Abstract

Altered cerebral metabolism and mitochondrial function have been identified in experimental and clinical studies of pediatric traumatic brain injury (TBI). Metabolic changes detected using 1H (proton) magnetic resonance spectroscopy correlate with long-Term outcomes in children after severe TBI. We previously identified early (4-h) and sustained (24-h and 7-day) abnormalities in brain metabolites after controlled cortical impact (CCI) in immature rats. The current study aimed to identify specific alterations of cerebral glucose metabolism at 24 h after TBI in immature rats. Rats (postnatal days 16-18) underwent CCI to the left parietal cortex. Sham rats underwent craniotomy only. Twenty-four hours after CCI, rats were injected (intraperitoneally) with [1,6-13C]glucose. Brains were removed, separated into hemispheres, and frozen. Metabolites were extracted with perchloric acid and analyzed using 1H and 13C-nuclear magnetic resonance spectroscopy. TBI resulted in decreases in N-acetylaspartate in both hemispheres, compared to sham contralateral. At 24 h after TBI, there was significant decrease in the incorporation of 13C label into [3-13C]glutamate and [2-13C]glutamate in the injured brain. There were no differences in percent enrichment of [3-13C]glutamate, [4-13C]glutamate, [3-13C]glutamine, or [4-13C]glutamine. There was significantly lower percent enrichment of [2-13C]glutamate in both TBI sides and the sham craniotomy side, compared to sham contralateral. No differences were detected in enrichment of 13C glucose label in [2-13C]glutamine, [2-13C]GABA (gamma-aminobutyric acid), [3-13C]GABA, or [4-13C]GABA, [3-13C]lactate, or [3-13C]alanine between groups. Results suggest that overall oxidative glucose metabolism in the immature brain recovers at 24 h after TBI. Specific reductions in [2-13C]glutamate could be the result of impairments in either neuronal or astrocytic metabolism. Future studies should aim to identify pathways leading to decreased metabolism and develop cell-selective "metabolic rescue."

Original languageEnglish (US)
Pages (from-to)2066-2072
Number of pages7
JournalJournal of neurotrauma
Volume30
Issue number24
DOIs
StatePublished - Dec 15 2013

Keywords

  • NMR spectroscopy
  • developmental brain injury
  • metabolism
  • mitochondria
  • trauma

ASJC Scopus subject areas

  • Clinical Neurology

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