Small, Jennifer Ruth; (1990) Sympathetic involvement in peripheral nerve injury. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

The aim of this study was to investigate the response of noradrenergic sympathetic efferent fibres to Injury In a peripheral nerve, and to attempt to elucidate the cytochemical basis for the abnormal Interaction between sympathetic efferent and sensory afferent fibres which develops in experimental neuromas. The painful nerve Injury model used throughout was the experimental neuroma. The numbers, distribution and morphological relationships of sympathetic efferent fibres in normal and injured rat sciatic nerve were studied. Noradrenaline (NA) was localized in fluorescence studies by a glyoxylic acid technique. Ultrastructural localization Involved treatment of animals with a monoamine oxidase Inhibitor, nialamide, followed by a 'false' transmitter, 5 - hydroxy dopamine (5-OH DA); or alternatively, cytochemical reaction according to a modified chromaffin technique, followed by x-ray microanalysis. Two pharmacological manipulations were employed. The first Involved treatment with guanethidine, a sympathetic blocking agent, and secondly, neonatally administered capsaicin, which selectively destroys afferent C fibres. The development of alpha adrenoreceptors and opiate receptors in the spinal cord, normal and transected sciatic nerves was studied, using autoradiography with tritiated para amino clonidine, an alpha-2 adrenoreceptor ligand and tritiated diprenorphine, an opiate receptor ligand. The fluorescence studies showed an accumulation of fluorescent material, NA, at the distal end of the proximal stump of the sectioned nerves, which was maximal 3 days after section. The number of sympathetic axons fell to below normal 14 days after section and returned towards normal by 8 weeks. NA could also be seen ultrastructurally, following pretreatment with nialamide and 5-OH DA, localized to electron-dense cored vesicles within sympathetic axons. Optimal localization of NA followed subsequent fixation in chromate containing fixative and electron probe x-ray microanalysis. Guanethidine treatment caused NA depletion, which was more marked in neuromas than normal nerves, especially at the distal tip of the proximal stumps, and varied between animals. Capsaicin treatment resulted in a loss of unmyelinated afferent axons, the effect being more obvious in the normal nerves. Autoradiographic studies showed a depletion of opiate receptors on the lesioned side of the spinal cord, but a slight Increase in the number of alpha adrenergic receptors on this side. The neuromas appeared to have increased numbers of both types of receptors when compared to the normal sciatic nerves, which were not labelled.

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