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The Journal of Neuroscience, September 15, 2001, 21(18):7194-7202

Insulin-Like Growth Factor-I Is Necessary for Neural Stem Cell Proliferation and Demonstrates Distinct Actions of Epidermal Growth Factor and Fibroblast Growth Factor-2

Yvan Arsenijevic^{1, 2}, Samuel Weiss³, Bernard Schneider¹, and Patrick Aebischer¹

¹ Division of Surgical Research and Gene Therapy Center, Pavillon 4 Centre Hospitalier Universitaire Vaudois, 1004 Lausanne, Switzerland, ² Unit of Oculogenetic, Eye Hospital Jules Gonin, 1004 Lausanne, Switzerland, and ³ Genes and Development Research Group, Department of Cell Biology and Anatomy, University of Calgary Faculty of Medicine, Calgary, Alberta, Canada T2N 4N1

Neural stem cells (NSCs), when stimulated with epidermal growth factor (EGF) or fibroblast growth factor-2 (FGF-2), have the capacity to renew, expand, and produce precursors for neurons, astrocytes, and oligodendrocytes. We postulated that the early appearance of insulin-like growth factor (IGF-I) receptors during mouse striatum development implies a role in NSC regulation. Thus, we tested in vitro the action of IGF-I on the proliferation of striatal NSCs. In the absence of IGF-I, neither EGF nor FGF-2 was able to induce the proliferation of E14 mouse striatal cells. However, addition of IGF-I generated large proliferative clusters, termed spheres, in a dose-dependent manner. The newly generated spheres were multipotent, and clonal analysis revealed that EGF or FGF-2, in the presence of IGF-I, acted directly on NSCs. The actions of IGF-I suggest distinct modes of action of EGF or FGF-2 on NSCs. First, continuous versus delayed administration of these neurotrophic factors showed that neither IGF-I nor EGF had an effect on NSC survival, whereas FGF-2 promoted the survival or maintenance of the stem cell state of 50% of NSCs for 6 d. Second, short-term exposure to IGF-I induced the proliferation of NSCs in the presence of EGF, but not of FGF-2, through an autocrine secretion of IGF-I. These findings suggest that IGF-I is a key factor in the regulation of NSC activation and that EGF and FGF-2 control striatal NSC proliferation, in part, through distinct intracellular mechanisms.

Key words: neurogenesis; neural stem cells; striatum; FGF-2; survival; autocrine regulation

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Copyright © 2001 Society for Neuroscience  0270-6474/01/21187194-09$05.00/0

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