Inflammatory pain mediated by a phenotypic switch in brain-derived neurotrophic factor-immunoreactive dorsal root ganglion neurons innervating the lumbar facet joints in rats.

Human low back pain sometimes originates from lumbar facet joints. In human lumbar facet joint inflammation or degeneration, the referred pain is not only expanded into the low back area but also into the leg or foot. The rat L5-L6 facet joint is innervated by the L1-L5 dorsal root ganglia. The presence of brain-derived neurotrophic factor-immunoreactive dorsal root ganglion neurons innervating the L5-L6 facet joint has been confirmed, but changes in the number and distribution of these neurons caused by inflammation have not been studied. Of fluorogold-labeled neurons innervating the L5-L6 facet joint, the proportion of brain-derived neurotrophic factor-immunoreactive dorsal root ganglion neurons was 16% in the control group and 26% in the inflammatory group. The proportion of brain-derived neurotrophic factor-immunoreactive dorsal root ganglion neurons labeled by fluorogold was significantly higher in the inflammatory group than in the control group (P<0.05). The mean cross-sectional area of fluorogold-labeled brain-derived neurotrophic factor-immunoreactive cells increased from 580 to 915 microm(2) in the inflammatory group (P<0.01). Associated with inflammation in facet joints, the increase of brain-derived neurotrophic factor-immunoreactive neurons and the phenotypic switch to large neurons may induce the expansion of facet joint inflammatory pain.