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Neurogenesis in Tα-1 tubulin transgenic mice during development and after injury
Journal article   Peer reviewed

Neurogenesis in Tα-1 tubulin transgenic mice during development and after injury

Turhan Coksaygan, Tim Magnus, Jingli Cai, Mohammed Mughal, Angelo Lepore, Haipeng Xue, Itzhac Fischer and Mahendra S. Rao
Experimental neurology, v 197(2), pp 475-485
2006
PMID: 16336967

Abstract

Development Glial precursor cells Neurons Stab wound injury
Tα-1 tubulin promoter-driven EYFP expression is seen in murine neurons born as early as E9.5. Double labeling with markers for stem cells (Sox 1, Sox 2, nestin), glial progenitors (S100β, NG2, Olig2), and neuronal progenitors (doublecortin, βIII-tubulin, PSA-NCAM) show that Tα-1 tubulin expression is limited to early born neurons. BrdU uptake and double labeling with neuronal progenitor markers in vivo and in vitro show that EYFP-expressing cells are postmitotic and Tα-1 tubulin EYFP precedes the expression of MAP-2 and NeuN, and follows the expression of PSA-NCAM, doublecortin (Dcx), and βIII-tubulin. Tα-1 tubulin promoter-driven EYFP expression is transient and disappears in most neurons by P0. Persistent EYFP expression is mainly limited to scattered cells in the subventricular zone (SVZ), rostral migratory stream, and hippocampus. However, there are some areas that continue to express Tα-1 tubulin in the adult without apparent neurogenesis. The number of EYFP-expressing cells declines with age indicating that Tα-1 tubulin accurately identifies early born postmitotic neurons throughout development but less clearly in the adult. Assessment of neurogenesis after stab wound injuries in the cortex, cerebellum and spinal cord of adult animals shows no neurogenesis in most areas with an increase in BrdU incorporation in glial and other non neuronal populations. An up-regulation of Tα-1 tubulin can be seen in certain areas unaccompanied by new neurogenesis. Our results suggest that even if stem cells proliferate their ability to generate neurons is limited and caution is warranted in attributing increased BrdU incorporation to stem cells or cells fated to be neurons even in neurogenic areas.

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Domestic collaboration
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Neurosciences
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