Overexpression of kynurenic acid in stroke: An endogenous neuroprotector?

It is known that kynurenic acid (KYNA) exerts a neuroprotective effect against the neuronal loss induced by ischemia; acting as a scavenger, and exerting antioxidant action. In order to study the distribution of KYNA, a highly specific monoclonal antibody directed against KYNA was developed. This distribution was studied in control rats and in animals in which a middle cerebral artery occlusion (stroke model) was induced. By double immunohistochemistry, astrocytes containing KYNA and GFAP were exclusively found in the ipsilateral cerebral cortex and/or striatum, at 2, 5 and 21 days after the induction of stroke. In control animals and in the contralateral side of the stroke animals, no immunoreactivity for KYNA was found. Under pathological conditions, the presence of KYNA is reported for the first time in the mammalian brain from early phases of stroke. The distribution of KYNA matches perfectly with the infarcted regions suggesting that, in stroke, this overexpressed molecule could be involved in neuroprotective/scavenger/antioxidant mechanisms.