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[Modification of redox sites of N-methyl-D-aspartate receptors affects changes in bioelectrical activity of olfactory cortex slices induced by anoxia in rats].

The effects of the thiol oxidative agent 5,5'-dithiobis (2-nitrobenzoic acid) (DTNB) inhibiting NMDA receptors activity on changes of the evoked focal potentials generation (the NMDA and non-NMDA components EPSP) in response to long-term (LA) and short-term (SA) anoxic exposure which induced functional disturbances or promoted increasing of neurons resistance to LA, were studied on the rat olfactory cortex slices (Wistar-Kyoto). It was revealed that DTNB (200 mkM) effectively protected the depression of the EPSP generation induced by LA in the most tested neurons. In addition, DTNB eliminates the protective effect of the SA on focal EPSP generation evoked by LA. Nevertheless this dependence concerns the NMDA component and, to a lesser extent, the non-NMDA component EPSP. A possible role of changes of the NMDA receptor modulatory redox sites in mechanisms of functional disturbances and increasing neuronal resistance induced by hypoxic influences, is discussed.