Dynamic roles of FGF-2 and Anosmin-1 in the migration of neuronal precursors from the subventricular zone during pre- and postnatal development

Diego García-González; Diego Clemente; Maria Coelho; Pedro F Esteban; Nadia Soussi-Yanicostas; Fernando de Castro

doi:10.1016/j.expneurol.2010.01.006

Dynamic roles of FGF-2 and Anosmin-1 in the migration of neuronal precursors from the subventricular zone during pre- and postnatal development

Exp Neurol. 2010 Apr;222(2):285-95. doi: 10.1016/j.expneurol.2010.01.006. Epub 2010 Jan 18.

Authors

Diego García-González¹, Diego Clemente, Maria Coelho, Pedro F Esteban, Nadia Soussi-Yanicostas, Fernando de Castro

Affiliation

¹ Grupo de Neurobiología del Desarrollo-GNDe, Unidad de Neurología Experimental, Hospital Nacional de Parapléjicos, Finca La Peraleda s/n, E-45071-Toledo, Spain.

PMID: 20083104
DOI: 10.1016/j.expneurol.2010.01.006

Abstract

FGF-2 and Anosmin-1 are diffusible proteins which act in cell proliferation and/or migration during CNS development. We describe their developmental expression patterns in the subventricular zone (SVZ) of the forebrain and the neuronal precursors (NPs) that migrate from this neurogenic site towards the olfactory bulb, forming the rostral migratory stream (RMS). The analysis is carried out before (E14), during (E17, P5) and after (P15) the peaks of migration along the RMS and before this acquires its mature conformation. At all these stages, FGF-2 exerts a FGFR1-mediated motogenic effect on NPs and induces the proliferation of SVZ astrocytes (putatively type B cells from triads), and Anosmin-1 works as a typical chemotropic agent for the NPs (mediated by FGFR1 at P5-P15). Altogether, our results are consistent with the notion that FGF-2 increases cell proliferation in the SVZ and would be the motogenic cue which feeds the migration of the newly produced NPs once generated, from early development (E14) and at least until P15, while Anosmin-1 cooperates in this migration attracting the NPs. In this sense, both cues should be considered as two of the first to be chronologically identified as actors in the formation of the RMS.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Animals, Newborn
Cell Movement / drug effects
Cell Movement / physiology*
Cell Proliferation
Cells, Cultured
Cerebral Ventricles* / cytology
Cerebral Ventricles* / enzymology
Cerebral Ventricles* / growth & development
Chemotaxis / drug effects
Chemotaxis / physiology
Coculture Techniques / methods
Embryo, Mammalian
Enzyme Inhibitors / pharmacology
Fibroblast Growth Factor 2 / genetics
Fibroblast Growth Factor 2 / metabolism*
Fibroblast Growth Factor 2 / pharmacology
Gene Expression Regulation, Developmental / drug effects
Gene Expression Regulation, Developmental / physiology*
Neoplasm Proteins
Nerve Tissue Proteins / genetics
Nerve Tissue Proteins / metabolism*
Nerve Tissue Proteins / pharmacology
Neural Cell Adhesion Molecule L1 / metabolism
Neurons / physiology*
Organ Culture Techniques
Rats
Rats, Wistar
Receptor, Fibroblast Growth Factor, Type 1 / metabolism
Sialic Acids / metabolism
Stem Cells / drug effects
Stem Cells / physiology*
Transfection / methods
Tubulin / metabolism

Substances

Enzyme Inhibitors
Neoplasm Proteins
Nerve Tissue Proteins
Neural Cell Adhesion Molecule L1
Sialic Acids
Tubulin
polysialyl neural cell adhesion molecule
Fibroblast Growth Factor 2
Wfdc18 protein, rat
Fgfr1 protein, rat
Receptor, Fibroblast Growth Factor, Type 1