Kainic acid rapidly induces cyclooxygenase (COX)-2 in piglet cerebral cortex

Ischemia/reperfusion (I/R) results in a robust induction of cyclooxygenase (COX)-2 in the newborn brain via unknown mechanisms, but glutamate release and activation of KA receptors may be involved. We examined effects of loca l KA (3-300 mu mol/l for 10 min) treatment on cortical COX-2 expression in anesthetized piglets using a closed cranial window. Treated and correspondi ng control tissue samples were collected 0.5-10 h after treatment. COX-2 mR NA and protein levels were assessed using RNase protection assay and immuno histochemistry, respectively. KA elicited reproducible dose-dependent incre ases in cortical COX-2 mRNA unaffected by indomethacin or N-G-nitro-L-argin ine methyl ester pretreatment. COX-2 mRNA levels were elevated at 30 min, p eaked at 2 h, but remained enhanced for up to 10 h after KA. Neuronal COX-2 immunoreactivity was also enhanced compared with the control side in all c ortical layers 8h after KA. In summary, activation of KA receptors may be i nvolved in the neuronal induction of COX-2 after I/R in the newborn. NeuroR eport 11:3435-3438 (C) 2000 Lippincott Williams & Wilkins.