Heat Hyperalgesia Induced by Endoneurial Nerve Growth Factor and the Expression of Substance P in Primary Sensory Neurons

Abstract

Endoneurial nerve growth factor (30 ng) produced significant heat hyperalgesia in rats on postinjection days 3 and 5. The percentage of neuron profiles expressing the sensory neuropeptide substance P in the dorsal root ganglion (DRG), and the density and distribution of substance P immunoreactivity at the DRG and the dorsal horn remained essentially unchanged throughout the 10 days of study. NGF increased pain scores in the second phase of the formalin test on postinjection day 3, but not on days 5 and 10. Our results indicate that the observed heat hyperalgesia is not dependent on NGF-induced changes in SP content and release from primary sensory neurons.

Nerve Growth Factor Contribution via Transient Receptor Potential Vanilloid 1 to Ectopic Orofacial Pain

“…Activation of downstream transcription factors by these MAPKs contributes to the transcriptional changes in sensory neurons that are associated with heat hyperalgesia (Ji et al, 2002). Indeed, retrograde NGF signaling from peripheral terminals in the inflamed tissue to the soma of nociceptive neurons enhances the expression of several proteins, such as TRPV1 (Delcroix et al, 2003), substance P (Yang et al, 2007;Ruiz and Baños, 2009), and brain-derived neurotrophic factor (BDNF) (Michael et al, 1997). NGF signaling also increases the anterograde transport of TRPV1 from the cell body to the peripheral terminals of nociceptors (Ji et al, 2002).…”