Present address: Laboratoire de Signalisation Cellulaire Normale et Tumorale, CNRS EP612, Université Montpellier I, Faculté de Pharmacie, 15 Avenue Charles Flahaut, 34060 Montpellier Cedex 1, France.
Potentiation of glutamatergic agonist-induced inositol phosphate formation by basic fibroblast growth factor is related to developmental features in hippocampal cultures: neuronal survival and glial cell proliferation
Article first published online: 26 AUG 2008
European Journal of Neuroscience
Volume 11, Issue 10, pages 3377–3386, October 1999
How to Cite
Blanc, E. M., Jallageas, M., Recasens, M. and Guiramand, J. (1999), Potentiation of glutamatergic agonist-induced inositol phosphate formation by basic fibroblast growth factor is related to developmental features in hippocampal cultures: neuronal survival and glial cell proliferation. European Journal of Neuroscience, 11: 3377–3386. doi: 10.1046/j.1460-9568.1999.00759.x
- Issue published online: 26 AUG 2008
- Article first published online: 26 AUG 2008
- Received 5 January 1999, revised 5 May 1999, accepted 10 May 1999
- AMPA receptors;
- in vitro development;
- metabotropic glutamate receptors;
- rat hippocampal cultures;
- trophic factors
We investigated the modulation by growth factors of phospholipase C (PLC)-linked glutamate receptors during in vitro development of hippocampal cultures. In defined medium, glial cells represent between 3 and 14% of total cell number. When we added basic fibroblast growth factor (bFGF) 2 h after plating, we found: (i) a neuroprotection from naturally occurring death for up to 5 days; (ii) a proliferation of glial cells from day 3; and (iii) a potentiation of quisqualate (QA)-induced inositol phosphate (IP) formation from 1 to 10 days in vitro (DIV) and 1s,3r-amino-cyclopentane-1,3-dicarboxylate (ACPD) response from 3 to 10 DIV. The antimitotic cytosine-β,d-arabinofuranoside (AraC) blocked glial cell proliferation induced by bFGF, but not neuroprotection. Under these conditions, the early potentiation of the QA response (1–3 DIV) was not changed, while the ACPD and late QA response potentiations were prevented (5–10 DIV). Epidermal growth factor was not neuroprotective but it induced both glial cell proliferation and late QA or ACPD potentiation. Surprisingly, the early bFGF-potentiated QA-induced IP response was blocked by 6,7-dinitro-quinoxaline-2,3-dione (DNQX), suggesting the participation of ionotropic (rs)-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate (KA) receptors. The delayed bFGF-potentiated ACPD-induced IP response is inhibited by (s)-α-methyl-4-carboxyphenylglycine (MCPG), indicating possible activation of glial metabotropic receptors. These results suggest that, in hippocampal cultures, bFGF modulates AMPA and metabotropic glutamate receptors linked to the IP cascade, possibly in relation to the regulation of neuronal survival and glial cell proliferation, respectively.