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Updated: Jan 27, 2026

Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording
Published on: August 11, 2019
Detrimental role of corticotropin-releasing factor on the decrease of CA1 field potential induced by in vitro
Yoshifumi Kagamiishi1, Tsuneyuki Yamamoto, Shigenori Watanabe
1Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Abstract:
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.
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