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Reichmann, F.
Signal transduction in primary sensory neurons
[ Diplomarbeit ] Medical University of Graz; 2009. pp. 43 [OPEN ACCESS]
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Authors Med Uni Graz:: Reichmann Florian
Advisor:: Donnerer Josef
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Abstract:: In the last few years phospho-ERK was the target of extensive research in the field of neuroscience. Especially the effect of various stimuli on the phosphorylation of ERK in sensory neurons was a central topic. It has been shown, that ERK can be activated by multiple noxious stimuli. The current work focuses on the activation of ERK by capsaicin. Capsaicin, the spicy ingredient of chilli peppers, induces the phosphorylation of ERK via the stimulation of primary afferent C-fibres mediated by the TRPV1 receptor. In the current experiment we investigated the pERK expression in the rat after capsaicin stimulation with the help of immunofluorescence microscopy. The aim of the study was to show, whether there is a difference of pERK levels in the dorsal root ganglion between groups stimulated with capsaicin and a control group. One of the capsaicin groups received capsaicin systemically and the other one received capsaicin perineurally, applied with a sponge wrapped around the sciatic nerve. After counting the strong fluorescent cells in the DRG we could show, that the number of pERK- positive cells was significantly higher in the capsaicin groups compared with the control group. In the systemic capsaicin group the mean of fluorescence producing cells was 11,1%, which is a significantly higher amount than 5,4% in the control group. Moreover there was a difference within the group, which received capsaicin perineurally. In this group the DRGs were separated into ipsilateral DRGs (on the same side where the capsaicin was applied onto the sciatic nerve) and contralateral DRGs. In this group the mean of strong fluorescence producing cells from the ipsilateral side was 9,2%, whereas the mean on the contralateral side was only 4,8%. This result was also significant. The increased phosphorylation of ERK following the capsaicin stimulation may be responsible for the development of hyperalgesia.