Age-related alterations in energy metabolism contribute to the increased vulnerability of the aging brain to anoxic damage

Eugene L. Roberts, Ching Ping Chih

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

Aging increases the vulnerability of brain tissue to anoxia and ischemia. We investigated whether age-related alterations in energy metabolism underlie this increased vulnerability. Energy metabolism was manipulated in hippocampal slices from Fischer 344 rats of ages 6-9 (young adult), 16-19 (middle-aged adult), and 26-29 (aged adult) months by altering glucose concentrations or by using lactate instead of glucose as the metabolic substrate. Extracellular K+ activity (Ko+) and synaptic excitability were monitored in stratum pyramidale of hippocampal subfield CA1. Aging diminished how well increasing concentrations of glucose delayed onset of anoxic depolarization and improved postanoxic recovery of Ko+ homeostasis and synaptic transmission. Hippocampal slices from all age groups responded to anoxia similarly when lactate was present instead of glucose. Also, no age-related differences were seen in normoxic ATP and phosphocreatine levels. These results suggest that an age-related decline in the glycolytic capacity of brain cells contributes to earlier onset of anoxic depolarization and poorer recovery of ion homeostasis and synaptic transmission in aging brain tissue.

Original languageEnglish (US)
Pages (from-to)83-90
Number of pages8
JournalBrain research
Volume678
Issue number1-2
DOIs
StatePublished - Apr 24 1995

Keywords

  • Anoxia
  • Brain slice
  • Glucose
  • Hippocampus
  • Hypoxia
  • Ion transport
  • Lactate
  • Synaptic transmission

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Age-related alterations in energy metabolism contribute to the increased vulnerability of the aging brain to anoxic damage'. Together they form a unique fingerprint.

Cite this