01877nab a2200349 a 4500003000900000005001700009008004100026041000800067100003400075700002700109245014900136264002700285300001600312500007200328520075800400650001701158650002101175650002201196650002301218650002001241650002001261650003101281650001901312650002901331650002201360773005901382942000801441035001701449001000701466999001901473040003501492AR-ReUNN20260702002328.0260630s1985    gw |||||||||||||||||eng  0 aeng1 aHuxtable, Clive R. R.91268401 aDorling, P. R.912684110aMannoside storage and axonal dystrophy in sensory neurones of swainsonine-treated rats: Morphogenesis of lesions / C. R. Huxtable; P. R. Dorling 1aBerlinbSpringerc1985  a9 páginas  aDisponible en http://www.springerlink.com/content/t9240715627620j1/  aSummary  Young rats were treated with swainsonine for up to 200 days at a dose rate that restricted neuronal mannoside storage to neurones not protected by the blood/brain barrier. In lumbar dorsal root ganglion neurones, mannoside storage in the cell body developed in parallel to dystrophic changes at the extremities of peripherally and centrally directed axons. The dystrophic process involved the accumulation of autophagic structures. In the CNS, axonal dystrophy was confined to areas receiving long processes from affected neurones. The results suggest that axonal dystrophy is a direct consequence of the lysosomal storage process in parent cell bodies. The possible relationship of axonal dystrophy to neuronal lysosomal function is discussed. 4aRata9117553 4aNeuronas9125042 4aDistrofia9126842 4aMorfogenesis99254 4aLesiones910073 4aMusculos938670 4aMorfología Animal962048 4aRoedores94076 4aExperimentación911630 4aSeparatas91209500 tActa Neuropatholx0001-6322gv. 68 n. 1 (1985)w223998  cART  a(AGROP)45835218766  c218766d218766  aAR-ReUNNbspacAR-ReUNNeaacr2