Early and sustained alterations in cerebral metabolism after traumatic brain injury in immature rats

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

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)603-614
Number of pages12
JournalJournal of neurotrauma
Volume25
Issue number6
DOIs
StatePublished - Jun 1 2008

Keywords

  • Development
  • Lactate
  • Mitochondria
  • N-Acetyl aspartate
  • NMR spectroscopy

ASJC Scopus subject areas

  • Clinical Neurology

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