Post-ischemic treatment with L-kynurenine sulfate exacerbates neuronal damage after transient middle cerebral artery occlusion

L. Gellért, L. Knapp, K. Németh, J. Herédi, D. Varga, G. Oláh, K. Kocsis, Á Menyhárt, Z. Kis, T. Farkas, L. Vécsei, J. Toldi

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Since brain ischemia is one of the leading causes of adult disability and death, neuroprotection of the ischemic brain is of particular importance. Acute neuroprotective strategies usually have the aim of suppressing glutamate excitotoxicity and an excessive N-methyl-d-aspartate (NMDA) receptor function. Clinically tolerated antagonists should antagonize an excessive NMDA receptor function without compromising the normal synaptic function. Kynurenic acid (KYNA) an endogenous metabolite of the tryptophan metabolism, may be an attractive neuroprotectant in this regard. The manipulation of brain KYNA levels was earlier found to effectively enhance the histopathological outcome of experimental ischemic/hypoxic states. The present investigation of the neuroprotective capacity of L-kynurenine sulfate (L-KYNs) administered systemically after reperfusion in a novel distal middle cerebral artery occlusion (dMCAO) model of focal ischemia/reperfusion revealed that in contrast with earlier results, treatment with L-KYNs worsened the histopathological outcome of dMCAO. This contradictory result indicates that post-ischemic treatment with L-KYNs may be harmful.

Original languageEnglish
Pages (from-to)95-101
Number of pages7
JournalNeuroscience
Volume247
DOIs
Publication statusPublished - Sep 5 2013

Keywords

  • Focal cerebral ischemia
  • Glycine co-agonist site
  • Kynurenines
  • MCAO model
  • NMDAR
  • Neuroprotection

ASJC Scopus subject areas

  • Neuroscience(all)

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