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At different post\u2010lesional time points (0.5, 1, 3, 6, 9 and 12\u00a0months) we used conventional electron microscopy and specific markers for astrocytes [glial fibrillary acidic protein (<jats:styled-content style=\"fixed-case\">GFAP<\/jats:styled-content>), vimentin (<jats:styled-content style=\"fixed-case\">V<\/jats:styled-content>im), sex\u2010determining region Y\u2010box\u20109 (<jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>ox9), paired box\u20102 (<jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>ax2)\u00b8 cluster differentiation\u201044 (<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>44)] and for proliferating cells (<jats:styled-content style=\"fixed-case\">PCNA<\/jats:styled-content>). The experimental retina showed a limited glial response since the increase of gliofilaments was not significant when compared with controls, and proliferating cells were undetectable. Conversely, <jats:styled-content style=\"fixed-case\">PCNA<\/jats:styled-content><jats:sup>+<\/jats:sup> cells populated the regenerating <jats:styled-content style=\"fixed-case\">ON<\/jats:styled-content>, optic tract (<jats:styled-content style=\"fixed-case\">OT<\/jats:styled-content>r) and ventricular wall of both the hypothalamus and optic tectum (<jats:styled-content style=\"fixed-case\">OT<\/jats:styled-content>). Subpopulations of these <jats:styled-content style=\"fixed-case\">PCNA<\/jats:styled-content><jats:sup>+<\/jats:sup> cells were identified as <jats:styled-content style=\"fixed-case\">GFAP<\/jats:styled-content><jats:sup>+<\/jats:sup> and Vim<jats:sup>+<\/jats:sup> reactive astrocytes and radial glia. Reactive astrocytes up\u2010regulated <jats:styled-content style=\"fixed-case\">V<\/jats:styled-content>im at 1\u00a0month post\u2010lesion, and both <jats:styled-content style=\"fixed-case\">V<\/jats:styled-content>im and <jats:styled-content style=\"fixed-case\">GFAP<\/jats:styled-content> at 12\u00a0months post\u2010lesion in the <jats:styled-content style=\"fixed-case\">ON<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">OT<\/jats:styled-content>r, indicating long\u2010term astrogliosis. They also expressed <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>ax2, <jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>ox9 and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>44 in the <jats:styled-content style=\"fixed-case\">ON<\/jats:styled-content>, and <jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>ox9 in the <jats:styled-content style=\"fixed-case\">OT<\/jats:styled-content>r. Concomitantly, persistent tissue cavities and disorganised regrowing fibre bundles reaching the <jats:styled-content style=\"fixed-case\">OT<\/jats:styled-content> were observed. Our ultrastructural data confirm abundant gliofilaments in reactive astrocytes joined by desmosomes. Remarkably, they also accumulated myelin debris and lipid droplets until late stages, indicating their participation in myelin removal. These data suggest that persistent mammalian\u2010like astrogliosis in the adult lizard <jats:styled-content style=\"fixed-case\">ON<\/jats:styled-content> contributes to a permissive structural scaffold for long\u2010term axonal regeneration and provides a useful model to study the molecular mechanisms involved in these beneficial neuron\u2013glia interactions.<\/jats:p>","DOI":"10.1111\/joa.12053","type":"journal-article","created":{"date-parts":[[2013,5,9]],"date-time":"2013-05-09T05:12:34Z","timestamp":1368076354000},"page":"22-37","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Regrowth of transected retinal ganglion cell axons despite persistent astrogliosis in the lizard (<i><scp>G<\/scp>allotia galloti<\/i>)"],"prefix":"10.1111","volume":"223","author":[{"given":"Mar\u00eda","family":"del Mar Romero\u2010Alem\u00e1n","sequence":"first","affiliation":[{"name":"Departamento de Morfolog\u00eda (Biolog\u00eda 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