Institutionen för odontologi

Examensarbete (30HP)

Examensarbete Tandhygienistutb.(30HP)

Examensarbete

Odontologi, magisteruppsats /D Examens år

Examensarbeten tandläkarutbildningen

 

2012
 
    Handledare:  Camilla Svensson och Per Alstergren

Chronic inflammation and pain – assessment of c-Fos and ATF-3 as markers of spinal neuronal activity in a pain model of rheumatoid arthritis

Nicole Nova
  

 


Chronic inflammatory pain in rheumatoid arthritis (RA) is a major clinical problem. RA factors induce constant noxious stimuli of peripheral nerves and spinal neurons, developing hypersensitivity and nociceptive pain, which persists subsequent to antiinflammatory treatment. The aim was to use the proto-oncogene protein c-Fos, the kinase pERK, and the transcription factor ATF-3 as markers to investigate spinal neuronal excitability during and after the inflammatory phase of RA, in order to explain the persistence of post-inflammatory chronic pain. Spinal cords of collagen antibody induced arthritis (CAIA) mice and age-matched control mice were cut and processed for immunohistochemistry. Immunoreactive neurons were located and quantified using fluorescence microscopy. The results showed that the increase in number of c-Fos immunoreactive neurons was most pronounced in the deep dorsal horn (DH) during the inflammatory phase, and less so after the peak of inflammation. Although the number of c-Fos positive neurons decreases when signs of arthritis disappear, the number is still elevated compared to the control. As for pERK, there were no active cells detected in CAIA or the control, and thus it was excluded from the study due to suspected experimental errors. Regarding ATF-3, there was no significant difference between CAIA and the control during and after the inflammatory phase. Further studies need to be undertaken to confirm these negative findings. In conclusion, the c-Fos expression in the spinal DH is elevated subsequent to induction of CAIA, indicating that arthritis induces long-term activation of DH neurons that persists even after the inflammation subsides. However, ATF-3 does not appear to be a good marker for neuronal excitability in the spinal cord for the CAIA mouse model.


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Artikel språk:Engelska