PURPOSE: The mechanism of hypoxic damage is mainly intracellular influx of calcium ions through the glutamate ionotropic receptor. This study was performed to determine alterations in distribution and expression of kainate receptor subunits after 1 hour of moderate hypoxia in the newborn piglet brain, as in a condition of mild to moderate perinatal hypoxic-ischemic encephalopathy. METHODS: Ten newborn piglets were ventilated at PaO2 over 80mmHg for 30min. Thereafter, the control group(n=5) was ventilated with 21% oxygen, and hypoxic group(n=5) with 6% oxygen at PaO2 below 25mmHg for 1 hour. Concentrations of protein, ATP and phosphocreatine were determined. The proteins were immunostained with anti-rat GluR6/7 and anti-rat KA2 antibody. RESULTS: Hypoxia(PaO2 20+/-1mmHg) and acidosis(pH 7.06+/-0.09) developed significantly in the hypoxic group compared to the control group(PaO2 104+/-4mmHg, pH 7.44+/-0.03, respectively, P<0.01). The concentrations of ATP(2.84+/-1.28micromol/kg brain, P<0.05) and phosphocreatine(0.78+/-1.07micromol/kg brain, P<0.001) were reduced compared to the control group(5.04+/-0.25micromol/kg brain, 4.03+/-0.31micromol/kg brain, respectively). The protein contents of GluR6/7 subunits were ordered; cerebral cortex>hippocampus, thalamus, hypothalamus>basal ganglia, cerebellum>white matter, and KA2 subunits were ordered : hippocampus, basal ganglia>cerebral cortex>thalamus, cerebellum>hypothalamus, white matter. The distribution of the subunits between the hypoxic group and control group were similar. CONCLUSION: Cerebral cortex, hippocampus and basal ganglia may be the most vulnerable to excitotoxic injury. Kainate receptor subunits did not change after 1 hour of moderate hypoxia.