Brain lactate uptake increases at the site of impact after traumatic brain injury

Tao Chen, Yong Zhen Qian, Ann Rice, Jie Pei Zhu, Xiao Di, Ross Bullock

Research output: Contribution to journalArticle

48 Scopus citations

Abstract

Although glucose is the main carbohydrate energy substrate for the normal brain, several studies published over the last 10 years now challenge this assumption. The activated brain increases its metabolism to meet increased energy demands by glycolysis after injury. In vitro studies now show that lactate alone can serve as an energy source to maintain synaptic function. In this study, we used 14C-lactate to test the hypothesis that blood lactate is acutely taken up by the injured brain, after fluid percussion injury (FPI) in the rat. 50 μCi radioactive lactate was injected i.v. immediately after FPI, in injured and sham rats. After 30 min, the brain was removed, frozen, and cut into 20 μm sections for autoradiography. Uptake of 14C-label was mainly concentrated at the injury site (2.5 times greater) although uninjured brain also took up the 14C-label. This increased concentration of radioactive lactate at the injury site suggests that the injured brain may use the lactate as an energy source. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)281-287
Number of pages7
JournalBrain Research
Volume861
Issue number2
DOIs
StatePublished - Apr 14 2000

Keywords

  • C-lactate
  • Energy
  • Fluid percussion injury

ASJC Scopus subject areas

  • Neuroscience(all)

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    Chen, T., Qian, Y. Z., Rice, A., Zhu, J. P., Di, X., & Bullock, R. (2000). Brain lactate uptake increases at the site of impact after traumatic brain injury. Brain Research, 861(2), 281-287. https://doi.org/10.1016/S0006-8993(00)01992-2