{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:38:28Z","timestamp":1786977508810,"version":"build-2736575974"},"reference-count":56,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2001,4,4]],"date-time":"2001-04-04T00:00:00Z","timestamp":986342400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Comparative Neurology"],"published-print":{"date-parts":[[2001,5,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The mechanisms of injury\u2010induced apoptosis of neurons within the CNS are not understood. We used a model of cortical injury in rat and mouse to induce retrograde neuronal apoptosis in thalamus. In this animal model, unilateral ablation of the occipital cortex causes unequivocal apoptosis of corticopetal projection neurons in the dorsal lateral geniculate nucleus (LGN) by 7 days postlesion. We tested the hypothesis that p53 and Bax regulate this retrograde neuronal apoptosis. We found, by using immunocytochemistry, that p53 accumulates in nuclei of neurons destined to undergo apoptosis. By immunoblotting, p53 levels increase (\u223c150% of control) in nuclear\u2010enriched fractions of the ipsilateral LGN by 5 days after occipital cortex ablation. p53 is functionally activated in nuclear fractions of the ipsilateral LGN at 5 days postlesion, as shown by DNA binding assay (\u223cfourfold increase) and by immunodetection of phosphorylated p53. The levels of procaspase\u20103 increase at 4 days postlesion, and caspase\u20103 is activated prominently at 5 days postlesion. To identify whether neuronal apoptosis in the adult brain is dependent on p53 and Bax, cortical ablations were done on\n                    <jats:italic>p53<\/jats:italic>\n                    and\n                    <jats:italic>bax<\/jats:italic>\n                    null mice. Neuronal apoptosis in the dorsal LGN is significantly attenuated (\u223c34%) in\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    mice. In lesioned\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>+\/+<\/jats:italic>\n                    <\/jats:sup>\n                    mice, Bax immunostaining is enhanced in the ipsilateral dorsal LGN and Bax immunoreactivity accumulates at perinuclear locations in dorsal LGN neurons. The enhancement and redistribution of Bax immunostaining is attenuated in lesioned\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    mice. Neuronal apoptosis in the dorsal LGN is blocked completely in\n                    <jats:italic>bax<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    mice. We conclude that neuronal apoptosis in the adult thalamus after cortical injury requires Bax and is modulated by p53. J. Comp. Neurol. 433:299\u2013311, 2001. \u00a9 2001 Wiley\u2010Liss, Inc.\n                  <\/jats:p>","DOI":"10.1002\/cne.1141","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T16:14:25Z","timestamp":1030292065000},"page":"299-311","source":"Crossref","is-referenced-by-count":56,"title":["Injury\u2010induced apoptosis of neurons in adult brain is mediated by p53\u2010dependent and p53\u2010independent pathways and requires bax"],"prefix":"10.1002","volume":"433","author":[{"given":"Lee J.","family":"Martin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adeel","family":"Kaiser","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan W.","family":"Yu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joanne 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