GLUTAMATE INDUCES IONOTROPIC AND METABOTROPIC GLUTAMATE RECEPTORS EXPRESSION IN PERIPHERAL MAST CELL POPULATIONS

Download or read book GLUTAMATE INDUCES IONOTROPIC AND METABOTROPIC GLUTAMATE RECEPTORS EXPRESSION IN PERIPHERAL MAST CELL POPULATIONS written by Magnus Peterson and published by . This book was released on 2017 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Background and aims: The peripheral nervous system exhibits a key role in regulating inflammation and pain signaling of the damaged tissue via afferent to efferent pathways. In a previous study, we used an Achilles tendon rupture rat model and showed that mast cells in the healing tendon were positive for the ionotropic glutamate receptor, NMDAR1. This raises the possibility that mast cells can be activated by glutamate release from peripheral nerve endings. Methods: We cultured mouse bone marrow derived mast cells (BMMC) and stimulated these cells with L-glutamate. Mast cell degranulation was quantified through u03b2-hexosaminidase release. We used immunofluorescence and Western blot techniques to quantify NMDARs and mgGluRs at the protein level, and RT-qPCR with microarray analysis to study the gene level expression. Results: We show that glutamate induces mast cell degranulation, and up-regulates the expression of glutamate receptors in mast cells. In agreement with this we found by qPCR and microarray analysis that mast cells upregulate the expression of a range of glutamate receptors in response to glutamate exposure, including ionotropic NMDAR1, NMDAR2A/2B, and metabotropic mGluR3, mGluR7. We also showed that the glutamate receptor, NMDAR1 co-localizes with glutamate in the cell membrane of mast cells exposed to glutamate, indicating the interaction between glutamate and its receptor(s) in the mast cell membrane.Conclusions: These findings introduce the possibility that glutamate signaling can have a functional impact on mast cells derived from peripheral tissue, suggesting a mechanism for neuro-immunological response.