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The Journal of Neuroscience, March 1, 2001, 21(5):1569-1579

Activation of Phosphatidylinositol-3 Kinase (PI-3K) and Extracellular Regulated Kinases (Erk1/2) Is Involved in Muscarinic Receptor-Mediated DNA Synthesis in Neural Progenitor Cells

Bing-Sheng Li¹, Wu Ma⁴, Lei Zhang³, Jeffery L. Barker², David A. Stenger⁴, and Harish C. Pant¹

¹ Laboratory of Neurochemistry and ² Laboratory of Neurophysiology, National Institute of Neurological Diseases and Stroke, and ³ Behavioral and Endocrinology Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, and ⁴ Center for Bio/Molecular Science and Engineering, Naval Research Laboratory, Washington, DC 20375

Muscarinic acetylcholine receptor (mAChR), a member of the G-protein-coupled receptors (GPCRs) gene superfamily, has been shown to mediate the effects of acetylcholine on differentiation and proliferation in the CNS. However, the mechanism or mechanisms whereby mAChRs regulate cell proliferation remain poorly understood. Here we show that in vitro bFGF-expanded neural progenitor cells dissociated from rat cortical neuroepithelium express muscarinic acetylcholine receptor subtype mRNAs. We demonstrate that stimulation of these mAChRs with carbachol, a muscarinic agonist, activated extracellular-regulated kinases (Erk1/2) and phosphatidylinositol-3 kinase (PI-3K). This, in turn, stimulated DNA synthesis in neural progenitor cells. MEK inhibitor PD98059 and PI-3K inhibitors wortmannin and LY294002 inhibited a carbachol-induced increase in DNA synthesis. These findings indicate that the activation of both PI-3 kinase and MEK signaling pathways via muscarinic receptors is involved in stimulating DNA synthesis in the neural progenitor cells during early neurogenesis.

Key words: progenitor cell; proliferation; muscarinic receptors; phosphorylation; protein kinase-B; MAP kinase

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Copyright © 2001 Society for Neuroscience  0270-6474/01/2151569-11$05.00/0

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