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Title: The role of galanin and neuropeptide Y in a rat model of neuropathic pain
Author: Colvin, L. A.
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1998
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Galanin and Neuropeptide Y (NPY) are not normally produced to any significant extent by primary afferent neurones. After peripheral nerve injury, however, there is a marked increase in their synthesis - galanin mainly in small to medium sized neurones, and NPY mainly in large neurones. There is evidence for transport of these newly produced peptides to the dorsal horn, but it is known what stimuli result in their release in the spinal cord. The antibody microprobe technique was therefore used to study the factors that might result in release of these peptides. The model that has been studied involved placement of four loose ligatures around one sciatic nerve in the rat, reliably resulting in the development of behavioural evidence of neuropathic pain. Microprobes bearing immobilised antibodies to galanin or NPY were inserted into the spinal cord of neuropathic rats. An increased area of galanin to release was detected in the superficial dorsal horn ipsilateral to nerve injury, as compared to controls. This occurred in the absence of any active peripheral stimulation, in an area of the dorsal horn encompassing the terminations of primary afferent fibres that have started to synthesise galanin. Galanin release was not increased by electrical stimulation of the injured nerve at a strength sufficient to activate A fibres, but there was an increase in release as C fibres were stimulated. Conduction block proximal to the dorsal root ganglia did not reduce spontaneous galanin release, and in fact, an increase was seen on the contralateral side of the cord. These studies have determined some of the stimuli responsible for the spinal release of galanin and NPY after peripheral nerve injury, and excluded others. Further work is required to correlate these results with functional effects and their possible role in the modulation of somatosensory, especially nociceptive, transmission.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available