Mitochondrial response to calcium in the developing brain

Courtney L. Robertson, Cynthia J. Bucci, Gary Fiskum

Research output: Contribution to journalArticlepeer-review

Abstract

Developmental differences in mitochondrial content and metabolic enzyme activities have been defined, but less is understood about the responses of brain mitochondria to stressful stimuli during development. Cerebral mitochondrial response to high Ca2+ loads after brain injury is a critical determinant of neuronal outcome. Brain mitochondria isolated from 16-18-day-old rats had lower maximal, respiration-dependent Ca2+ uptake capacity than brain mitochondria isolated from adult rats in the presence of ATP at both a pH of 7.0 and 6.5. However, in the absence of ATP, immature brain mitochondria exhibited greater Ca2+ uptake capacity at pH 7.0 and 6.5, indicating a greater resistance of immature brain mitochondria to Ca2+-induced dysfunction under conditions relevant to those that exist during acute ischemic and traumatic brain injury. Acidosis reduced the maximal Ca2+ uptake capacity in both immature and adult brain mitochondria. Cytochrome c was released from both immature and adult brain mitochondria in response to Ca2+ exposure, but was not affected by cyclosporin A, an inhibitor of the mitochondrial membrane permeability transition. Developmental changes in mitochondrial response to Ca2+ loads may have important implications in the pathobiology of brain injury to the developing brain.

Original languageEnglish (US)
Pages (from-to)141-148
Number of pages8
JournalDevelopmental Brain Research
Volume151
Issue number1-2
DOIs
StatePublished - Jul 19 2004
Externally publishedYes

Keywords

  • Acidosis
  • Brain mitochondria
  • Cytochrome c
  • Development
  • Development and regeneration
  • Neuronal death

ASJC Scopus subject areas

  • Developmental Neuroscience
  • Developmental Biology

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