Evidence that synaptically-released zinc contributes to neuronal injury after traumatic brain injury

Sang Won Suh, Jefferson W. Chen, Massoud Motamedi, Bell Brent Bell, Kathy Listiak, Neus F. Pons, Gorm Danscher, Christopher J. Frederickson

Research output: Contribution to journalArticle

248 Scopus citations

Abstract

Prior evidence indicates that synaptically-released zinc enters postsynaptic neurons in toxic excess during ischemia and seizures. In addition, prevention of this zinc translocation has been shown to be neuroprotective in both ischemia and seizures. Here we show evidence that the same translocation of zinc from presynaptic boutons into postsynaptic neurons occurs after mechanical injury to the brain. Specifically, using a rat model of traumatic brain injury, we show that trauma is associated with (i) loss of zinc from presynaptic boutons (ii) appearance of zinc in injured neurons, and (iii) neuroprotection by intraventricular administration of a zinc chelator just prior to brain impact. The possible use of zinc chelators for neuroprotection after head trauma is considered. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)268-273
Number of pages6
JournalBrain Research
Volume852
Issue number2
DOIs
StatePublished - Jan 10 2000

Keywords

  • AMG
  • Brain trauma
  • Hippocampus
  • TSQ
  • Zinc

ASJC Scopus subject areas

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

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