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Crosstalk between neurons and satellite glial cells in sensory ganglia during peripheral tissue inflammation

Grant number: 16/07838-8
Support type:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): October 10, 2016
Effective date (End): October 09, 2017
Field of knowledge:Biological Sciences - Physiology - General Physiology
Principal researcher:Carlos Amilcar Parada
Grantee:Amanda Ferreira Neves
Supervisor abroad: Stephen David Roper
Home Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Research place: University of Miami, United States  
Associated to the scholarship:13/08678-6 - THE ROLE OF P2X7 RECEPTORS PRESENT IN SENSORY GANGLIA IN PAIN INDUCED BY PERIPHERAL TISSUE INFLAMMATION, BP.DR

Abstract

Our work has provided evidences on the involvement of satellite glial cells (SGC) from dorsal root ganglion (DRG) in the development of inflammatory hyperalgesia in peripheral tissue as result of a communication with neurons. We have previously demonstrated that during inflammation of peripheral tissue, the development of inflammatory hyperalgesia depends on the activation of interleukin-1 receptor 1 (IL-1R1) on primary afferent neurons in peripheral tissue, which in turn induces the release of interleukin-1 beta (IL-1b) in DRG. In the current PhD project we demonstrated that ATP released by neurons and activation of P2X7 receptor expressed by SGC mediates this release of IL-1b in DRG. In other words, the activation of peripheral IL-1 receptor on primary afferent neurons induces the release of ATP in DRG that activates P2X7 receptor from surrounding SGC. Then, ATP-induced P2X7 receptor activation leads to cleavage and release of mature IL-1b in DRG, but not the synthesis of IL-1b by SGC. However, it is not clear the mechanism underlying the increase of IL-1b synthesis in SGC following the inflammatory process in peripheral tissue. There is evidence that IL-1b in peripheral tissue can increase the excitability of primary afferent neuron by modulating NMDA receptor. Also, chemical or electrical stimulation of primary afferent neuron induces the releasing of substance P and glutamate in addition to ATP. Because SGC have receptors to substance P and NMDA, it is plausible to hypothesize that these neuronal mediators may participate of the crosstalk between primary afferent nociceptor and SGC to induce IL-1b synthesis in SGC during peripheral inflammatory stimulus. Therefore, the aim of this work is to use in vivo confocal imaging and specific biosensor cells in dorsal root ganglion to: (1) confirm that administration of IL-1b in peripheral tissue and activation of IL-1R1 on primary afferent neurons induces the release of ATP in DRG; (2) verify if inflammatory stimuli in peripheral tissue induce the release of glutamate and substance P in DRG that activate NDMA and substance P receptors of SGC to upregulate IL-1b synthesis in these cells. (AU)

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