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Effects of graded experimental compression on slow and fast axonal transport in rabbit vagus nerve
Authors:L B Dahlin  W G McLean
Affiliation:1. Laboratory of Experimental Biology, Department of Anatomy, University of Gothenburg, Gothenburg Sweden;2. Department of Pharmacology and Therapeutics, University of Liverpool, Liverpool U.K.;1. Institute of Primary Care & Public Health, Cardiff University School of Medicine, Neuadd Meirionnydd, Heath Park, Cardiff, UK;2. The Scar Free Foundation Centre for Children’s Burn Research, Bristol Royal Hospital for Children, University Hospitals Bristol NHS Foundation Trust, BS2 8BJ, UK;3. Centre for Child and Adolescent Health, School of Social and Community Medicine, University of Bristol, Oakfield House, Oakfield Grove, Bristol BS8 2BN, UK;4. University of the West of England, Coldharbour Lane, Frenchay, Bristol BS16 1QY, UK;1. Photonics Research Centre, University of Malaya, 50603 Kuala Lumpur, Malaysia;2. Microelectronics & Nanotechnology-Shamsuddin Research Centre (MiNT-SRC), University Tun Hussein Onn Malaysia, 86400 Parit Raja, Batu Pahat, Johor, Malaysia;3. Faculty of Electrical and Electronic Engineering, University Tun Hussein Onn Malaysia, 86400 Parit Raja, Batu Pahat, Johor, Malaysia
Abstract:Effects of compression at low pressures on slow and fast axonal transport was investigated in rabbit vagus nerve. Proteins in the sensory fibres were radiolabelled by injection of [3H]leucine or [35S]methionine into the nodose ganglion. A small compression chamber and/or ligatures were applied around the cervical part of the vagus nerve for 8 h, at an appropriate time for the subsequent analysis of the effects of compression on both slow and fast transport of radiolabelled proteins. In normal nerves there were two waves of slowly transported proteins with rates of about 12-15 and 25-30 mm/day, respectively. SDS-polyacrylamide gel electrophoresis was used and confirmed that the main proteins which accumulated proximal to the ligatures had a molecular weight of 54 000-56 000. Neither compression of the nerve at 20 mm Hg nor sham-compression induced any statistically significant accumulation of slowly transported proteins at the site of compression. A higher pressure, i.e. 30 mm Hg, induced a marked but incomplete accumulation of slowly transported proteins. Fast transport was partially inhibited in some, but not all, nerves, when 20 mm Hg was applied for 8 h, in contrast to the lack of effect found previously with the same pressure applied for only 2 h. Despite these slight differences, the results indicate that both slow and fast transport are impaired by low pressure levels of around 20-30 mm Hg, which are comparable with those found in human compression neuropathies. The impaired provision of cytoskeletal elements to the distal axon may be of significance in the pathophysiology of nerve entrapment syndromes.
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