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The Journal of Neuroscience, August 17, 2005, 25(33):7636-7647; doi:10.1523/JNEUROSCI.0485-05.2005

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Cellular/Molecular
Retinoic Acid Signaling Identifies a Distinct Precursor Population in the Developing and Adult Forebrain

Gloria Thompson Haskell^1,2 and Anthony-Samuel LaMantia¹

¹Department of Cell and Molecular Physiology and ²Curriculum in Neurobiology and University of North Carolina Neuroscience Center, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina 27599

We asked whether retinoic acid (RA), an established transcriptional regulator in regenerating and developing tissues, acts directly on distinct cell classes in the mature or embryonic forebrain. We identified a subset of slowly dividing precursors in the adult subventricular zone (SVZ) that is transcriptionally activated by RA. Most of these cells express glial fibrillary acidic protein, a smaller subset expresses the epidermal growth factor receptor, a few are terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling positive, and they can be mitotically labeled by sustained rather than acute bromodeoxyuridine exposure. RA activation in similar cells in SVZ-derived neurospheres depends on retinoid synthesis from the premetabolite retinol. The apparent influence of RA on precursors in vitro is consistent with key properties of RA activation in the SVZ; in neurospheres, altered retinoid signaling elicits neither cell death nor an acute increase in cell proliferation. There is apparent continuity of RA signaling in the forebrain throughout life. RA-activated, proliferative precursors with radial glial characteristics are found in the dorsal lateral ganglionic eminence and ventrolateral palliumembryonic rudiments of the SVZ. Thus, endogenous RA signaling distinguishes subsets of neural precursors with glial characteristics in a consistent region of the adult and developing forebrain.

Key words: forebrain; glia; neural precursor; olfactory bulb; subventricular zone; retinoic acid

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Received Feb 4, 2005; revised June 10, 2005; accepted June 28, 2005.

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