{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T07:08:39Z","timestamp":1790665719944,"version":"4.1.0"},"reference-count":36,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2008,12,29]],"date-time":"2008-12-29T00:00:00Z","timestamp":1230508800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Glia"],"published-print":{"date-parts":[[2009,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The primary sources of cortical gliogenesis, either during development or after adult brain injury, remain uncertain. We previously generated Nestin\u2010CreER mice to fate\u2010map the progeny of radial glial cells (RG), a source of astrocytes and oligodendrocytes in the nervous system. Here, we show that Nestin\u2010CreER mice label another population of glial progenitors, namely the perinatal subventricular zone (SVZ) glioblasts, if they are crossed with stop\u2010floxed EGFP mice and receive tamoxifen in late embryogenesis (E16\u2013E18). Quantification showed E18 tamoxifen\u2010induction labeled more perinatal SVZ glioblasts than RG and transitional RG combined in the newborn brain (54% vs. 22%). Time\u2010lapse microscopy showed SVZ\u2010glioblasts underwent complex metamorphosis and often\u2010reciprocal transformation into transitional RG. Surprisingly, the E10\u2010dosed RG progenitors produced astrocytes, but no oligodendrocytes, whereas E18\u2010induction fate\u2010mapped both astrocytes and NG2+ oligodendrocyte precursors in the postnatal brain. These results suggest that cortical oligodendrocytes mostly derive from perinatal SVZ glioblast progenitors. Further, by combining genetic fate\u2010mapping and BrdU\u2010labeling, we showed that cortical astrocytes cease proliferation soon after birth (&lt;P10) and only undergo nonproliferative gliosis (i.e., increased GFAP expression without cell\u2010division) after stab\u2010wound injury in adult brains. By contrast, 9.7% of cortical NG2+ progenitors remained mitotic at P29, and the ratio rose to 13.8% after stab\u2010wound injury. Together, these results suggest NG2+ progenitors, rather than GFAP+ astrocytes, are the primary source of proliferative gliosis after adult brain injury. \u00a9 2008 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/glia.20835","type":"journal-article","created":{"date-parts":[[2008,12,31]],"date-time":"2008-12-31T19:44:24Z","timestamp":1230752664000},"page":"1115-1129","source":"Crossref","is-referenced-by-count":61,"title":["Developmental and post\u2010injury cortical gliogenesis: A Genetic fate\u2010mapping study with Nestin\u2010CreER mice"],"prefix":"10.1002","volume":"57","author":[{"given":"Kevin A.","family":"Burns","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"Murphy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steve C.","family":"Danzer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chia\u2010Yi","family":"Kuan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2008,12,29]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/glia.20121"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(04)00140-0"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/glia.20519"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0709002105"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1093\/cercor\/bhl164"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1242\/dev.02847"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3545-08.2008"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.10-02-00684.1990"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1044-7431(03)00210-0"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1002\/cne.901240105"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4499-05.2006"},{"key":"e_1_2_6_13_1","first-page":"55","volume-title":"Glial 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