Inhibitory role of d-series resolvins in the cellular response to painful stimuli in trigeminal ganglion neurons

Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.Resolvins (Rv) are molecules that are responsible for the active resolution of inflammation. Recent studies have suggested that the resolvins are capable of inhibiting pain associated with inflammation. Our goal was to determine the effects of RvD1, aspirin triggered (AT)-RvD1, and RvD2 on the intracellular calcium concentration ([Ca2+]i) response to the painful stimulus, capsaicin, in cultured trigeminal ganglion neurons. Neuronal cells of the rat trigeminal ganglia were isolated and cultured on 35 mm glass bottom dishes that had been treated with poly-D lysine and laminin. Cells were incubated in the presence or absence of RvD1 , RvD2, or AT-RvD1. Cells were then loaded with Fura-2 to detect changes in [Ca2+]i..[Ca2+]i was measured in response to capsaicin administration. RvD1, AT-RvD1, and RvD2 significantly inhibited the increase in [Ca2+]i in response to capsaicin. In addition the localization of lipoxin A4 (ALX) receptor that can be used by RvD1 and AT-RvD1 and nestin that indicates neurons was detected in the plated cells using immunofluorescence microscopy. The ability of D-series resolvins to inhibit the Ca2+i response to capsaicin suggests that this type of resolvin has the potential to be effective endogenous analgesics in pain conditions of the face and head. The presence of the ALX receptor on the cells of the trigeminal ganglion supports the hypothesis that RvD1 and AT-RvD1 could inhibit pain through interaction with ALX