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To address this discrepancy, we used immunohistochemistry to analyze the expression of CNTF receptor \u03b1 (CNTFR\u03b1) in mouse retina and optic nerve following intraorbital nerve crush. In normal mice, RGC perikarya and axons were intensely labeled for CNTFR\u03b1. At 24 hours after crush, the immunoreactivity normally seen on axons in the nerve was lost near the lesion. This loss radiated from the crush site with time. At 2 days postlesion, labeled axons were not detected in the proximal nerve, and at 2 weeks were barely detectable in the retina. In the distal nerve, loss of axonal staining progressed to the optic chiasm by 7 days and remained undetectable at 2 weeks. Interfascicular glia in the normal optic nerve were faintly labeled, but by 24 hours after crush they became intensely labeled near the lesion. Double labeling showed these to be both astrocytes and oligodendrocytes. At 7 days postlesion, darkly labeled glia were seen throughout the optic nerve, but at 14 days labeling returned to normal. It is suggested that the loss of CNTFR\u03b1 from axons renders RGCs unresponsive to CNTF, thereby contributing to regenerative failure and death, while its appearance on glia may promote glial scarring. J. Comp. Neurol. 500:384\u2013400, 2007. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/cne.21174","type":"journal-article","created":{"date-parts":[[2006,11,17]],"date-time":"2006-11-17T21:47:23Z","timestamp":1163800043000},"page":"384-400","source":"Crossref","is-referenced-by-count":27,"title":["Immunohistochemical localization of CNTFR\u03b1 in adult mouse retina and optic nerve following intraorbital nerve crush: Evidence for the axonal loss of a trophic factor receptor after injury"],"prefix":"10.1002","volume":"500","author":[{"given":"Jill A.","family":"Miotke","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. 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