The experiments were performed on incubated slices of the rat rostal olfactory cortex. The slices were treated with various concentrations (10(-7) to 10(-9)) of corticotropin-releasing factor before (40 min), during, and after a 10-minute anoxic episode. The parallel control experiments were carried out without CRF. A 10-minute anoxia, both in control experiments and in perfusion with CRF, resulted in an approximately equal decrease of field excitatory postsynaptic potential's (fEPSP) amplitude. However, CRF at 10 nM and 100 nM concentrations protected the fEPSP amplitude. The selected NMDA receptor antagonists 2-amino-5-phosphonopentanoate (AP5) added in the perfusion medium after the anoxia, did not eliminate the neuroprotective effect of CRF.