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The Journal of Neuroscience, March 9, 2005, 25(10):2687-2701; doi:10.1523/JNEUROSCI.0951-04.2005

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Cellular/Molecular
Canonical Transient Receptor Potential 1 Plays a Role in Basic Fibroblast Growth Factor (bFGF)/FGF Receptor-1-Induced Ca²+ Entry and Embryonic Rat Neural Stem Cell Proliferation

Alessandra Fiorio Pla,¹ Dragan Maric,¹ So-Ching Brazer,³ Paolo Giacobini,^2,4 Xibao Liu,³ Yoong Hee Chang,¹ Indu S. Ambudkar,³ and Jeffery L. Barker¹

¹Laboratory of Neurophysiology and ²Cellular and Developmental Neurobiology Section, National Institute of Neurological Disorders and Stroke, and ³Secretory and Physiology Section, Gene Therapy and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892, and ⁴Department of Human and Animal Biology, University of Torino, 10123 Torino, Italy

Basic fibroblast growth factor (bFGF) and its major receptor FGF receptor-1 (FGFR-1) play an important role in the development of the cortex. The mechanisms underlying the mitogenic role of bFGF/FGFR-1 signaling have not been elucidated. Intracellular Ca²⁺ concentrations ([Ca²⁺]_i) in proliferating cortical neuroepithelial cells are markedly dependent on Ca²⁺ entry (Maric et al., 2000a). The absence of voltage-dependent Ca²⁺ entry channels, which emerge later, indicates that other membrane mechanisms regulate [Ca²⁺]_i during proliferation. Canonical transient receptor potential (TRPC) family channels are candidates because they are voltage independent and are expressed during CNS development (Strübing et al., 2003).

Here, we investigated the involvement of TRPC1 in bFGF-mediated Ca²⁺ entry and proliferation of embryonic rat neural stem cells (NSCs). Both TRPC1 and FGFR-1 are expressed in the embryonic rat telencephalon and coimmunoprecipitate. Quantitative fluorescence-activated cell sorting analyses of phenotyped telencephalic dissociates show that 80% of NSCs are TRPC1⁺, proliferating, and express FGFR-1. Like NSCs profiled ex vivo, NSC-derived progeny proliferating in vitro coexpress TRPC1 and FGFR1. Antisense knock-down of TRPC1 significantly decreases bFGF-mediated proliferation of NSC progeny, reduces the Ca²⁺ entry component of the Ca_i²⁺ response to bFGF without affecting Ca²⁺ release from intracellular stores or 1-oleoyl-2-acetyl-sn-glycerol-induced Ca²⁺ entry, and significantly blocks an inward cation current evoked by bFGF in proliferating NSCs. Both Ca²⁺ influx evoked by bFGF and NSC proliferation are attenuated by Gd³⁺ and SKF96365 two antagonists of agonist-stimulated Ca²⁺ entry. Together, these results show that TRPC1 contributes to bFGF/FGFR-1-induced Ca²⁺ influx, which is involved in self-renewal of embryonic rat NSCs.

Key words: calcium [Ca]; cortex; development; proliferation; TRPC; neural stem cells

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Received March 15, 2004; revised January 27, 2005; accepted January 31, 2005.

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