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Fibroblast growth factor 2 (FGF2) is involved in hippocampus-dependent learning. In this study, the effects of FGF2 on the excitability were investigated in granule cells of rat dentate gyrus. Hippocampal slices were used to perform patch clamp recordings in granule cells. Extracellularly applied FGF2 early quenched the depolarization-induced repetitive firing, suggesting a decreased excitability under these conditions. Consistently, transient and sustained voltage-gated K(+) currents decreased in a dose-dependent manner, repolarization phase of action potential was slowed down, afterhyperpolarization was reduced, and membrane resistance was decreased. These effects were not mediated by tyrosine kinase FGF2 receptors. Moreover, an involvement of G protein signaling was ruled out, as well as an intracellular action of FGF2. Considering the relationship between FGF2 and hippocampal functions, the modulation of neuron excitability by activity-driven FGF2 release may be regarded as a part of a homeostatic mechanism of self-regulation of hippocampal activity.

In the dentate gyrus of the mammalian hippocampus, neurogenesis carries on throughout postnatal life. The aim of this work was to identify an exogenous control factor of adult neurogenesis. Neurogenesis in the adult dentate gyrus was previously found to be enhanced in vitamin E-deficient rats. The effects of alpha- or beta-tocopherol supplementation on neurogenesis in the adult dentate gyrus were investigated by 5-bromo-2'-deoxyuridine labeling. Tocopherol was found to increase the survival of newborn cells and the total number of granule cells in the adult rat dentate gyrus. Newborn cells were phenotypically characterized by expression of the immature neuron marker TOAD-64 (turned on after division-64). Therefore tocopherol in high doses possibly increases the number of granule cells in the dentate gyrus by saving newborn cells from death.

Abstract: Fibroblast growth factor 2 (FGF2) is involved in hippocampus-dependent learning. In this study, the effects of FGF2 on the excitability were investigated in granule cells of rat dentate gyrus. Hippocampal slices were used to perform patch clamp recordings in granule cells. Extracellularly applied FGF2 early quenched the depolarization-induced repetitive firing, suggesting a decreased excitability under these conditions. Consistently, transient and sustained voltage-gated K+ currents decreased in a dose-dependent manner, repolarization phase of action potential was slowed down, afterhyperpolarization was reduced, and membrane resistance was decreased. These effects were not mediated by tyrosine kinase FGF2 receptors. Moreover, an involvement of G protein signaling was ruled out, as well as an intracellular action of FGF2. Considering the relationship between FGF2 and hippocampal functions, the modulation of neuron excitability by activity-driven FGF2 release may be regarded as a part of a homeostatic mechanism of self-regulation of hippocampal activity. [Copyright &y& Elsevier]