Fig. 8From: Glial interleukin-1β upregulates neuronal sodium channel 1.7 in trigeminal ganglion contributing to temporomandibular joint inflammatory hypernociception in ratsDiagram of glial IL-1β-induced upregulation of neuronal Nav1.7 contributed to TMJ inflammatory hypernociception through the COX-2/PGE2/EP2-evoked PKA/CREB signaling pathway. TMJ inflammation somehow activates SGCs, which activate the transcriptions of IL-1β and COX-2 leading to increase in PGE2 release from the SGCs to subsequently activate the neuronal EP2/PKA/CREB signaling pathway then leading to upregulation of Nav1.7 in neurons and finally the increase in the neuronal excitability, which amplifies the stimuli in the TMJ contributing to the development of TMJ inflammatory hypernociception. TG, trigeminal ganglion; N, neuron; SGC, satellite glial cellsBack to article page