scholarly journals Postnatal Neurogenesis in the Subventricular Zone: A Manipulable Source for CNS Plasticity and Repair

Author(s):  
Manavendra Pathania ◽  
Angelique Bordey
2015 ◽  
Vol 37 (2) ◽  
pp. 115-130 ◽  
Author(s):  
Beth A. Costine ◽  
Symeon Missios ◽  
Sabrina R. Taylor ◽  
Declan McGuone ◽  
Colin M. Smith ◽  
...  

Stimulation of postnatal neurogenesis in the subventricular zone (SVZ) and robust migration of neuroblasts to the lesion site in response to traumatic brain injury (TBI) is well established in rodent species; however, it is not yet known whether postnatal neurogenesis plays a role in repair after TBI in gyrencephalic species. Here we describe the anatomy of the SVZ in the piglet for the first time and initiate an investigation into the effect of TBI on the SVZ architecture and the number of neuroblasts in the white matter. Among all ages of immaturity examined the SVZ contained a dense mesh network of neurogenic precursor cells (doublecortin+) positioned directly adjacent to the ependymal cells (ventricular SVZ, Vsvz) and neuroblasts organized into chains that were distinct from the Vsvz (abventricular SVZ, Asvz). Though the architecture of the SVZ was similar among ages, the areas of Vsvz and Asvz neuroblast chains declined with age. At postnatal day (PND) 14 the white matter tracts have a tremendous number of individual neuroblasts. In our scaled cortical impact model, lesion size increased with age. Similarly, the response of the SVZ to injury was also age dependent. The younger age groups that sustained the proportionately smallest lesions had the largest SVZ areas, which further increased in response to injury. In piglets that were injured at 4 months of age and had the largest lesions, the SVZ did not increase in response to injury. Similar to humans, swine have abundant gyri and gyral white matter, providing a unique platform to study neuroblasts potentially migrating from the SVZ to the lesioned cortex along these white matter tracts. In piglets injured at PND 7, TBI did not increase the total number of neuroblasts in the white matter compared to uninjured piglets, but redistribution occurred with a greater number of neuroblasts in the white matter of the hemisphere ipsilateral to the injury compared to the contralateral hemisphere. At 7 days after injury, less than 1% of neuroblasts in the white matter were born in the 2 days following injury. These data show that the SVZ in the piglet shares many anatomical similarities with the SVZ in the human infant, and that TBI had only modest effects on the SVZ and the number of neuroblasts in the white matter. Piglets at an equivalent developmental stage to human infants were equipped with the largest SVZ and a tremendous number of neuroblasts in the white matter, which may be sufficient in lesion repair without the dramatic stimulation of neurogenic machinery. It has yet to be determined whether neurogenesis and migrating neuroblasts play a role in repair after TBI and/or whether an alteration of normal migration during active postnatal population of brain regions is beneficial in species with gyrencephalic brains.


Development ◽  
2020 ◽  
Vol 147 (10) ◽  
pp. dev184861
Author(s):  
Astrid Deryckere ◽  
Elke Stappers ◽  
Ruben Dries ◽  
Elise Peyre ◽  
Veronique van den Berghe ◽  
...  

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
William W Hwang ◽  
Ryan D Salinas ◽  
Jason J Siu ◽  
Kevin W Kelley ◽  
Ryan N Delgado ◽  
...  

The epigenetic mechanisms that enable specialized astrocytes to retain neurogenic competence throughout adult life are still poorly understood. Here we show that astrocytes that serve as neural stem cells (NSCs) in the adult mouse subventricular zone (SVZ) express the histone methyltransferase EZH2. This Polycomb repressive factor is required for neurogenesis independent of its role in SVZ NSC proliferation, as Ink4a/Arf-deficiency in Ezh2-deleted SVZ NSCs rescues cell proliferation, but neurogenesis remains defective. Olig2 is a direct target of EZH2, and repression of this bHLH transcription factor is critical for neuronal differentiation. Furthermore, Ezh2 prevents the inappropriate activation of genes associated with non-SVZ neuronal subtypes. In the human brain, SVZ cells including local astroglia also express EZH2, correlating with postnatal neurogenesis. Thus, EZH2 is an epigenetic regulator that distinguishes neurogenic SVZ astrocytes, orchestrating distinct and separable aspects of adult stem cell biology, which has important implications for regenerative medicine and oncogenesis.


Glia ◽  
2016 ◽  
Vol 64 (9) ◽  
pp. 1465-1478 ◽  
Author(s):  
Monica Benito-Muñoz ◽  
Carlos Matute ◽  
Fabio Cavaliere

2011 ◽  
Vol 85 (3-4) ◽  
pp. 169-179 ◽  
Author(s):  
Sandra Guidi ◽  
Patrizia Bianchi ◽  
Aage K. Olsen Alstrup ◽  
Kim Henningsen ◽  
Donald F. Smith ◽  
...  

2020 ◽  
Vol 30 (7) ◽  
pp. 4092-4109 ◽  
Author(s):  
Mariyam Akter ◽  
Naoko Kaneko ◽  
Vicente Herranz-Pérez ◽  
Sayuri Nakamura ◽  
Hisashi Oishi ◽  
...  

Abstract Even after birth, neuronal production continues in the ventricular–subventricular zone (V–SVZ) and hippocampus in many mammals. The immature new neurons (“neuroblasts”) migrate and then mature at their final destination. In humans, neuroblast production and migration toward the neocortex and the olfactory bulb (OB) occur actively only for a few months after birth and then sharply decline with age. However, the precise spatiotemporal profiles and fates of postnatally born neurons remain unclear due to methodological limitations. We previously found that common marmosets, small nonhuman primates, share many features of V–SVZ organization with humans. Here, using marmosets injected with thymidine analogue(s) during various postnatal periods, we demonstrated spatiotemporal changes in neurogenesis during development. V–SVZ progenitor proliferation and neuroblast migration toward the OB and neocortex sharply decreased by 4 months, most strikingly in a V–SVZ subregion from which neuroblasts migrated toward the neocortex. Postnatally born neurons matured within a few months in the OB and hippocampus but remained immature until 6 months in the neocortex. While neurogenic activity was sustained for a month after birth, the distribution and/or differentiation diversity was more restricted in 1-month-born cells than in the neonatal-born population. These findings shed light on distinctive features of postnatal neurogenesis in primates.


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