NEUROPROTECTIVE EFFECT OF HYPOTHERMIA IN CORTICAL CULTURES EXPOSED TOOXYGEN-GLUCOSE DEPRIVATION OR EXCITATORY AMINO-ACIDS

We examined the effect of moderate hypothermia (30 degrees C) on neuro nal injury in murine cortical cell cultures. Lowering the temperature during and after a period of oxygen-glucose deprivation reduced both t he release of glutamate to the bathing medium and accompanying neurona l degeneration. Hypothermia immediately after brief exposure to high c oncentrations of NMDA or glutamate also reduced the resulting neuronal degeneration. This protective effect was not eliminated when MK-801 a nd 6-cyano-7-nitroquinoxaline-2,3-dione were added immediately after w ashout of the exogenously added excitotoxin, suggesting that it was me diated by actions additional to reduction of endogenous late glutamate release. Hypothermia applied only during exposure to NMDA or glutamat e, whether brief or prolonged, did not reduce subsequent cytosolic cal cium accumulation or neuronal degeneration, suggesting that the postsy naptic induction of NMDA receptor-mediated excitotoxicity is not sensi tive to temperature reduction. However, hypothermia during prolonged l pha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid or kainate expo sure did reduce neuronal degeneration.