L5 spinal nerve ligation in rats increased VR1 expression in spared L4 DRG neurons from day 1 to 28, corresponding with thermal hyperalgesia, while P2X3 expression remained unchanged.
In a rat model of neuropathic pain, VR1 but not P2X3 expression increases in spared L4 DRG neurons, correlating with thermal hyperalgesia.
We investigated the expression of two candidate transducers of noxious stimuli in peripheral tissues, the vanilloid receptor subtype 1 (VR1) and the P2X(3), a subunit of the ionotropic P2X receptor for ATP, in spared L4 DRG neurons following L5 spinal nerve ligation, a neuropathic pain model. VR1 mRNA expression increased in the small- and medium-sized DRG neurons from the first to 28th day after injury, and this up-regulation corresponded well with the development and maintenance of thermal hyperalgesia of the hind paw. The increase in VR1-immunoreactive (ir) neurons was confirmed at the third day after surgery. In contrast, there was no change in expression of P2X(3) mRNA over 4 weeks after ligation, or in the percentage of P2X(3)-ir neurons observed 3 days after surgery. Our data suggests that increased VR1 in the spared L4 DRG may contribute to the exaggerated heat response observed in this neuropathic pain model. Taken together with the previous reports that P2X(3) expression increases in the spared DRG neurons in other neuropathic pain models, there appears to be differences in the phenotypic changes and pathomechanisms of the various neuropathic pain models.
Fukuoka et al. (Sun,) conducted a other in Neuropathic pain (L5 spinal nerve ligation model). L5 spinal nerve ligation was evaluated on Expression of VR1 and P2X3 in spared L4 DRG neurons. L5 spinal nerve ligation in rats increased VR1 expression in spared L4 DRG neurons from day 1 to 28, corresponding with thermal hyperalgesia, while P2X3 expression remained unchanged.