FGF2 modulates the voltage-dependent K+ current and changes excitability of rat dentate gyrus granule cells

• Published in: Neuroscience letters Vol. 462; no. 3; pp. 203 - 206
• Main Authors: Cuppini, Carla, Ambrogini, Patrizia, Lattanzi, Davide, Ciuffoli, Stefano, Cuppini, Riccardo
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 25.09.2009; Elsevier
• Subjects: Action Potentials; Animals; Biological and medical sciences; Cell excitability; Dentate gyrus; Dentate Gyrus - physiology; FGF2; Fibroblast Growth Factor 2 - physiology; Fundamental and applied biological sciences. Psychology; In Vitro Techniques; K+ current; Male; Neurons - physiology; Patch-Clamp Techniques; Potassium Channels, Voltage-Gated - physiology; Rat; Rats; Rats, Sprague-Dawley; Vertebrates: nervous system and sense organs; Dentate gyrus; Rat; FGF2; Cell excitability; K+ current; Granule neuron; Rodentia; Central nervous system; Excitability; Basic fibroblast growth factor; K; Encephalon; Vertebrata; current; Mammalia; Animal; Potassium; Hippocampus
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2009.07.029

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.