Cyclosporin ameliorates traumatic brain-injury-induced alterations of hippocampal synaptic plasticity

Benedict C. Albensi, Patrick G. Sullivan, Michael B. Thompson, Stephen W. Scheff, Mark P. Mattson

Research output: Contribution to journalArticlepeer-review

Abstract

Although traumatic brain injury (TBI) often results in impaired learning and memory functions, the underlying mechanisms are unknown and there are currently no treatments that can preserve such functions. We studied plasticity at CA3-CA1 synapses in hippocampal slices from rats subjected to controlled cortical impact TBI. Long-term potentiation (LTP) of synaptic transmission was markedly impaired, whereas long-term depression (LTD) was enhanced, 48 h following TBI when compared to unoperated and sham control rats. Post-TBI administration of cyclosporin A, a compound that stabilizes mitochondrial function, resulted in a highly significant amelioration of the impairment of LTP and completely prevented the enhancement of LTD. Our data suggest that alterations in hippocampal synaptic plasticity may be responsible for learning and memory deficits resulting from TBI and that agents such as cyclosporin A that stabilize mitochondrial function may be effective treatments for TBI. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)385-389
Number of pages5
JournalExperimental Neurology
Volume162
Issue number2
DOIs
StatePublished - Apr 2000
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Apoptosis
  • Learning and memory
  • Long-term depression
  • Long-term potentiation
  • Mitochondrial permeability transition

ASJC Scopus subject areas

  • Neurology
  • Neuroscience(all)

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