Abstract
This study investigated the hypothesis that activation of satellite glial cells modulates the excitability of trigeminal ganglion (TRG) neuronal activity via an IL-1β following inflammation. Two days post-CFA injection, the mean percentage of TRG neurons encircled by glial fibrillary acidic protein (GFAP)- / IL-1β-immunoreactive cells was significantly increased compared to controls. GFAP and IL-1β immunoreactivities were co-expressed in the same cells. Fluorogold (FG) labeling identified the site of inflammation. The number of FG-labeled IL-receptor type I (IL-1RI) TRG neurons in inflamed rats was significantly greater than in controls. In FG-labeled small TRG neurons, the size of IL-1β (1 nM) induced-depolarization in inflamed rats was larger than in controls. IL-1β application significantly increased firing rates evoked by depolarizing pulses in the neurons of inflamed rats,compared to controls. Inhibition of voltage-dependent K+ currents by IL-1β application in inflamed rats was significantly larger than in control. The responses of TRG neuronal activity to IL-1β were abolished by treatment with the IL-1RI antagonist. These results suggest that activation of satellite glial cells modulates the excitability of small-diameter TRG neurons via IL-1β following inflammation, and that the up-regulation of IL-1RI in the soma may contribute to the mechanism underlying inflammatory hyperalgesia. [J Physiol Sci. 2007;57 Suppl:S111]
