A latent neurogenic program in astrocytes regulated by Notch signaling in the mouse

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Science  10 Oct 2014:
Vol. 346, Issue 6206, pp. 237-241
DOI: 10.1126/science.346.6206.237

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Neurogenesis is restricted in the adult mammalian brain; most neurons are neither exchanged during normal life nor replaced in pathological situations. We report that stroke elicits a latent neurogenic program in striatal astrocytes in mice. Notch1 signaling is reduced in astrocytes after stroke, and attenuated Notch1 signaling is necessary for neurogenesis by striatal astrocytes. Blocking Notch signaling triggers astrocytes in the striatum and the medial cortex to enter a neurogenic program, even in the absence of stroke, resulting in 850 ± 210 (mean ± SEM) new neurons in a mouse striatum. Thus, under Notch signaling regulation, astrocytes in the adult mouse brain parenchyma carry a latent neurogenic program that may potentially be useful for neuronal replacement strategies.

Astrocytes' hidden ability to generate neurons

New neurons could be useful in the brain to respond to damage done by disease, trauma, or just plain age. But the adult brain does not produce many new neurons. Working in mice, Magnusson et al. hunted for intrinsic genetic programs that can help adult brains produce replacement neurons. They found that astrocytes, spidery cells that are interspersed between neurons, carry a latent neurogenic program. The ability to entice astrocytes to replace neurons could obviate the need for neuronal replacement strategies.

Science, this issue p. 237

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