EN
Despite of many years of research, the evidence for interactions between the peripheral nervous system and the immune system remains incomplete. Our recent studies have shown that the proinflammatory cytokines interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF) play a critical role in the pathogenesis of the immune response within the peripheral endings of trigeminal ganglion neurons. The goal of the current project was to determine whether peripheral inflammation leads to changes in BDNF expression in trigeminal ganglia. In order to examine the effects of peripheral inflammation on the regulation of BDNF content in trigeminal ganglion neurons in vivo, a model of CFA-evoked inflammation in the TMJ of C57BL mice was employed. BDNF levels in trigeminal ganglia ipsilateral to the CFA-induced inflammation were compared with BDNF levels in the control ganglia from the contralateral (intact) side, on day 3 and 7 after induction of inflammation. A standard sandwich ELISA methodology was used to compare levels of BDNF in the trigeminal ganglion that supplies the tissue that has been affected by the inflammatory process with BDNF levels in the contralateral ganglion. These in vivo data further support the notion that BDNF is a likely key player of trigeminal inflammatory pain.