Premium
Neuronal survival and calcium influx induced by basic fibroblast growth factor in chick ciliary ganglion neurons
Author(s) -
Distasi Carla,
Torre Marina,
Antoniotti Susanna,
Munaron Luca,
Lovisolo Davide
Publication year - 1998
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1998.00239.x
Subject(s) - ciliary ganglion , neuroscience , ganglion , calcium , basic fibroblast growth factor , nerve growth factor , biology , fibroblast growth factor , microbiology and biotechnology , anatomy , medicine , growth factor , receptor
Basic fibroblast growth factor (bFGF/FGF2) exhibits widespread biological activities in the nervous system. However, little is known about the cascade of intracellular events that links the activation of its tyrosine kinase receptors to these effects. Here we report that, in ciliary ganglion neurons from chick embryo, this trophic factor significantly enhanced neuronal survival. The percentage of surviving neurons was reduced when intracellular calcium was chelated by adding a membrane‐permeable BAPTA ester to the culture medium, while antagonists of L‐ and N‐type voltage‐dependent calcium channels were ineffective. The ionic signals in response to bFGF stimulation have been studied using cytofluorimetric and patch‐clamp techniques. In single‐cell Fura‐2 measurements, bFGF elicited a long lasting rise of the cytosolic calcium concentration that was dependent on [Ca 2+ ] o . In whole‐cell experiments, we observed a reversible depolarization of the membrane resting potential and an inward cationic current. Single channel experiments, performed in the cell‐attached configuration, provide evidence for the activation of two families of Ca 2+ ‐permeable cationic channels. Moreover, inositol 1,4,5‐trisphosphate opens channels with similar properties, suggesting that this cytosolic messenger can be responsible for the calcium influx induced by bFGF.