The International Association for the Study of Pain (IASP) defines pain as "an unpleasant sensory and emotional experience, associated with actual or potential tissue damage, or described in terms of such damage". When the pain is originated by an inflammation, it can be considered as the result of the interaction between the damaged tissue and peripheral nociceptive sensory neurons. On the other hand, neuropathic pain can be caused by any lesions in the somatosensory system. In these types of pain, plastic changes throughout the nociceptive sensory system are associated with the chronification of the pain process. The observed plasticity results from the induction and/or repression of several genes that are modulated by the activation of different transcription factors. One of the key transcription factors known so far is the activator protein-1 (AP-1), which is related to the regulation of a variety of cellular processes such as proliferation, growth, differentiation, apoptosis and cell migration. However, the role of AP-1 in the induction and maintenance of chronic pain processes is not well established yet. Through behavioral experiments, along with molecular biology techniques, this project's main objective is to test the hypothesis that the activation of transcription factor AP-1 plays a crucial role in the genesis of persistent and neuropathic inflammatory pain. We will focus on the possible role of AP-1 in the production of proinflammatory cytokines on spinal level and the dorsal root ganglia and their possible role in the induction of metalloproteinases 2 and 9, which has been characterized as essential to the genesis of these types of pain.
News published in Agência FAPESP Newsletter about the scholarship: