Abstract

Neural stem cells (NSCs) in the walls of the lateral ventricles continue to produce new neurons and oligodendrocytes throughout life. The identification of NSCs, long-range neuronal migration, and the integration of new neurons into fully formed mature neural circuits—all in the juvenile or adult brain—has dramatically changed concepts in neurodevelopment and suggests new strategies for brain repair. Yet, the latter has to be seen in perspective: NSCs in the adult are heterogeneous and highly regionally specified; young neurons derived from these primary progenitors migrate and integrate in specific brain regions. Neurogenesis appears to have a function in brain plasticity rather than brain repair. If similar processes could be induced in regions of the brain that are normally not a target of new neurons, therapeutic neuronal replacement may one day reinstate neural circuit plasticity and possibly repair broken neural circuits.

Highlights

  • Neural stem cells (NSCs) in the walls of the lateral ventricles continue to produce new neurons and oligodendrocytes throughout life

  • This dogma began to change with observations made by Joseph Altman in the 1960’s: [H]3-thymidine labeled progenitors gave rise to cells in several brain regions that had the morphology of neurons under the light microscope (Altman, 1962)

  • From the early observations in mammals and songbirds, to the more recent work in the mammalian hippocampus and the ventricular-subventricular zone (V-SVZ), adult neurogenesis has been proclaimed to offer a new hope for brain repair (Nottebohm, 1985; Gage and Temple, 2013)

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Summary

Introduction

Neural stem cells (NSCs) in the walls of the lateral ventricles continue to produce new neurons and oligodendrocytes throughout life. In the adult rodent V-SVZ a subpopulation of progenitors with astroglial characteristics, known as B1 cells, function as the NSCs. B1 cells generate young neurons that migrate long distances via the rostral migratory stream (RMS) to the OB where they differentiate into local circuit GABAergic interneurons.

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Conclusion

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