Axonal Transport in Human Nerve Disease and in the Experimental Neuropathy Induced by p-Bromophenylacetylurea
Authors:
- 1 January 1982
- book chapter
- Published by Springer Nature in Proceedings in Life Sciences
- p. 124-130
Abstract
No abstract availableKeywords
This publication has 18 references indexed in Scilit:
- Axonal transport of enzymes and labeled proteins in experimental axonopathy induced by p-bromophenylacetylureaBrain Research, 1981
- ‘Acrylamide-induced‘ neuropathy and impairment of axonal transport of proteins. II. Abnormal accumulations of smooth endoplasmic reticulum as sites of focal retention of fast transported proteins. Electron microscope radioautographic studyBrain Research, 1981
- Direct comparison of the rapid axonal transport of norepinephrine and dopamine-?-hydroxylase activityJournal of Neurobiology, 1977
- Stop-flow: A new technique for measuring axonal transport, and its application to the transport of dopamine-β-hydroxylaseJournal of Neurobiology, 1975
- Axonal Transport of Dopamine-β-Hydroxylase by Human Sural Nerves in vitroScience, 1973
- AXOPLASMIC FLOW IN AXONAL NEUROPATHIES I. AXOPLASMIC FLOW IN CATS WITH TOXIC NEUROPATHIESBrain, 1973
- The effect of DFP on axonal transport of protein in chicken sciatic nerveBrain Research, 1970
- “NEUROAXONAL DYSTROPHY” OCCURRING IN AN EXPERIMENTAL, “DYING BACK” PROCESS IN THE RATBrain, 1969
- The experimental neuropathy in rats caused by p-bromophenylacetylurea.Journal of Neurology, Neurosurgery & Psychiatry, 1968
- Nervensch digung durch p-Bromphenylacetyl-HarnstoffNaunyn-Schmiedeberg's Archives of Pharmacology, 1960