On the early toxic effect of quinolinic acid: Involvement of RAGE

Elvis Cuevas, Susan Lantz, Glenn Newport, Becky Divine, Qiangen Wu, Merle G. Paule, J. César Tobón-Velasco, Syed F. Ali, Abel Santamaría

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Quinolinic acid (QUIN)-induced toxicity is characterized by N-methyl-d-aspartate receptors over-activation, excitotoxicity and oxidative damage. The characterization of toxic cascades produced by QUIN during the first hours after its striatal infusion is relevant for understanding toxic mechanisms. The role of the receptor-for-advanced-glycation-end-products (RAGE) in the early toxic pattern induced by QUIN was evaluated. RAGE expression - assessed by Western blot analysis and immunofluorescence - was enhanced in the striata of QUIN-lesioned rats at 2. h post-lesion. QUIN-induced RAGE up-regulation was accompanied by expression of a RAGE target molecule, nuclear factor kappa B (NF-κB), and genes encoding for different enzymes. Other toxic markers linked to RAGE activation were increased by QUIN, including NO formation, premature glial response, lactate dehydrogenase leakage, mitochondrial dysfunction and nuclear condensation. Our results suggest that RAGE up-regulation may play a role in the early stages of QUIN toxicity.

Original languageEnglish (US)
Pages (from-to)74-78
Number of pages5
JournalNeuroscience Letters
Volume474
Issue number2
DOIs
StatePublished - Apr 2010
Externally publishedYes

Keywords

  • Huntington's disease
  • NF-κB
  • Neurodegeneration
  • Neurotoxicity
  • Oxidative stress
  • Quinolinic acid
  • Receptor-for-advanced-glycation-end-products

ASJC Scopus subject areas

  • General Neuroscience

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