S100β protects hippocampal neurons from damage induced by glucose deprivation

Steven W. Barger, Linda J. Van Eldik, Mark P. Mattson

Research output: Contribution to journalArticlepeer-review

126 Scopus citations

Abstract

S100β is a calcium-binding protein elevated in Down's syndrome and Alzheimer's disease. Previous studies have demonstrated that S100β is trophic for several neuronal populations. We tested the influence of S100β on hippocampal neurons. The initial response included a rapid increase in [Ca2+]i similar to that elicited by S100β in other populations. S100β also substantially decreased cell death and loss of mitochondrial function resulting from glucose deprivation. Therefore, S100β exerts a neuroprotective influence on CNS neurons, suggesting that its elevation in neurological disorders may be a compensatory response.

Original languageEnglish
Pages (from-to)167-170
Number of pages4
JournalBrain Research
Volume677
Issue number1
DOIs
StatePublished - Apr 17 1995

Bibliographical note

Funding Information:
This work was supported in part by funds from the NIH (S.W.B., M.P.M., and L.V.E.), the Alzheimer's Association (M.P.M.), and the French Foundation (S.W.B.). We are grateful to Stefan Strack for helpful discussion.

Keywords

  • Calcium
  • Glucose
  • Hippocampus
  • Mitochondria
  • Neurotrophic
  • S100

ASJC Scopus subject areas

  • General Neuroscience
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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