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. 2000 May 29;149(5):1157–1166. doi: 10.1083/jcb.149.5.1157

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© 2000 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Axonal degeneration and demyelination are exacerbated in tPA-deficient mice after sciatic nerve crush. Oil Red O staining of cryostat sections of uninjured wild-type sciatic nerve (A) revealed normal myelin distribution, and toluidine blue staining of sciatic nerve semi-thin cross-sections showed normal axon morphology (B). 8 d after crush (cd8), toluidine blue staining of semi-thin cross-sections of wild-type mice (C) demonstrated more myelinated axons (arrows) than tPA^−/− mice (D). Oil Red O staining showed increased accumulation of myelin and lipid debris in the tPA^−/− (F) compared with the wild-type (E) sciatic nerve. 22 d after crush (cd22), staining for myelin basic protein revealed fewer myelinated axons in tPA^−/− (H) than in wild-type (G) nerves. Bar, 18 μm.