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Detrimental role of corticotropin-releasing factor on the decrease of CA1 field potential induced by in vitro ischemia in rat hippocampal slices.

This experiment was designed to test the hypothesis that endogenous corticotropin-releasing factor (CRF) contributes to the neurodegenerative process following an ischemic insult. To test this hypothesis, the effects of chronic intracerebroventricular administration of CRF or astressin, a CRF-receptor antagonist, on the decrease in the Schaffer collateral-CA1 field potential induced by hypoxia/hypoglycemia (ischemia), were tested in rat hippocampal slices. The chronic treatment with CRF had a significant exacerbating effect on the 10-min ischemia, a condition that did not affect the evoked synaptic response in the hippocampal CA1 area, as compared to vehicle-treated rats. On the other hand, astressin had a significant ameliorative effect on the 15-min ischemia-induced reduction of the evoked synaptic response in the hippocampal CA1 area. These findings suggest that CRF accelerates hippocampal ischemic vulnerability induced by hypoxia and hypoglycemia.