No abstract

Experiments were performed to address the dynamics of evoked focal potentials in slices of rat olfactory cortex during 10-min anoxia and subsequent reoxygenation. These experiments showed that perfusion with corticotropin-releasing factor (CRF)--corticoliberin--at concentrations of 1, 10, and 100 nM had no effect on changes in EPSP parameters before or during anoxia. However, CRF (10 and 100 nM) significantly aided recovery of the amplitude and slope of EPSP during reoxygenation. Application of the competitive NMDA receptor blocker APV (50 microM) during reoxygenation did not eliminate the protective effects of CRF on neuronal activity.

We studied the effect of in vivo hypobaric hypoxia on the development (after 3 h) of in vitro long-term posttetanic potentiation in Wistar rats. Severe hypoxia suppressed induction of posttetanic potentiation in slices of the olfactory cortex. Preconditioning exposure (moderate hypobaric hypoxia) prevented inhibition of posttetanic potentiation induced by severe hypoxia.

Experiments were performed to investigate evoked focal potentials in slices of rat olfactory cortex. The results showed that 1 microM corticotropin-releasing factor (CRF; corticoliberin) increases the frequency of posttetanic potentiation, which had a shorter delay phase than in control experiments. Posttetanic potentiation during perfusion with 0.1 microM corticoliberin had a longer delay phase than in control experiments.