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Journal of Neuroscience, Vol 16, 2649-2658, Copyright © 1996 by Society for Neuroscience
In vivo growth factor expansion of endogenous subependymal neural precursor cell populations in the adult mouse brain
CG Craig, V Tropepe, CM Morshead, BA Reynolds, S Weiss and D van der Kooy
Deparment of Anatomy and Cell Biology, University of Toronto, Ontario, Canada.
The lateral ventricle subependyma in the adult mammalian forebrain contains
both neural stem and progenitor cells. This study describes the in situ
modulation of these subependymal neural precursor populations after
intraventricular administration of exogenous growth factors. In vivo
infusion of epidermal growth factor (EGF) into adult mouse forebrain for 6
consecutive days resulted in a dramatic increase in the proliferation and
total number of subependymal cells and induced their migration away from
the lateral ventricle walls into adjacent parenchyma. Immediately after EGF
infusion, immunohistochemical characterization of the EGF-expanded cell
population demonstrated that >95% of these cells were EGF receptor- and
nestin-positive, whereas only 0.9% and 0.2% labeled for astrocytic and
neuronal markers, respectively. Seven weeks after EGF withdrawal, 25% of
the cells induced to proliferate after 6d of EGF were still detectable; 28%
of these cells had differentiated into new astrocytes and 3% into new
neurons in the cortex, striatum, and septum. Newly generated
oligodendrocytes were also observed. These in vivo results (1) confirm the
existence of EGF-responsive subependymal neural precursor cells in the
adult mouse forebrain and (2) suggest that EGF acts directly as a
proliferation, survival, and migration factor for subependymal precursor
cells to expand these populations and promote the movement of these cells
into normal brain parenchyma. Thus, in situ modulation of endogenous
forebrain precursor cells represents a novel model for studying neural
development in the adult mammalian brain and may provide insights that will
achieve adult replacement of neurons and glia lost to disease or trauma.
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