Advanced search
Start date

Study of cells involved in the prostaglandin-E2-release in the dorsal root ganglion during inflammatory hyperalgesia

Grant number: 13/03789-4
Support Opportunities:Scholarships in Brazil - Post-Doctoral
Effective date (Start): September 01, 2013
Effective date (End): May 31, 2014
Field of knowledge:Biological Sciences - Physiology
Principal Investigator:Carlos Amilcar Parada
Grantee:Dionéia Araldi
Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil


Results from our laboratory have shown that the development of inflammatory hyperalgesia in peripheral tissue depends on the synthesis and release of prostaglandins (PGs) in dorsal root ganglion (DRG). However these results did not clarify which cells of the DRG, among satellite cells, neurons TRPV1 peptidergic and non-peptidergic, are involved in this phenomenon. In a therapeutic perspective, the development of drugs, in particular nonsteroidal anti-inflammatory drugs (NSAIDs), which act selectively on a target cells, is an exciting proposal. For that, the identification of the cells that synthesize and release prostaglandins in the DRG involved in the inflammatory hyperalgesia in tissue peripheral is crucial. The identification of such cells would allow the development of prototype drugs conjugated with specific drug delivery systems, which could address NSAIDs to selective DRG cells to selectively inhibit the cyclooxygenase (COX), and thereby, providing an analgesic effect with reduced side effects. Thus, the aim of this study is to investigate the relative participation of DRG cells (peptidergic, non-peptidergic or satellite cells) in the synthesis and release of prostaglandins in DRG, which one is involved in the development of inflammatory hyperalgesia of peripheral tissue.

News published in Agência FAPESP Newsletter about the scholarship:
Articles published in other media outlets (0 total):
More itemsLess items

Please report errors in scientific publications list using this form.