Date of this Version
Redwine, A., Romereim, S., & Wachs, R. (2020, April). Quantification of phenotypic change resulting in sensitization of primary sensory neurons due to oxidative stress. Poster submission online for UCARE at the University of Nebraska-Lincoln, Lincoln, NE.
84% of the population will suffer from low back pain at some point in their lives, and 39% of the cases may be related to pain originating from the intervertebral disc (IVD) also known as discogenic pain. Age or injury can cause progressive degeneration of the IVD, and this can allow innervation by nociceptive (pain-sensing) neurons from the dorsal root ganglion (DRG) into the inner IVD.6 Long-term exposure to pain-inducing stimuli can cause nociceptor sensitization, manifested as increased pain sensation in response to non-painful or painful stimuli.7 Sensitization results in the nociceptors responding more strongly to a stimulus, and the activation energy required for response is reduced.8 During IVD degeneration, inflammation and oxidative stress create excess reactive oxygen species (ROS) .9 ROS such as superoxide may play a role in nociceptive signaling and lead to nociceptor sensitization.8 ROS are involved in the chronic pain that results from nerve injury or inflammation in many contexts and may be involved in discogenic pain as well.10 The focus of this study is to determine if long-term oxidative stress causes a change in the DRG nociceptive neuron phenotype related to sensitization. This would increase the expression of pain-related ion channels and lower the neuronal activation threshold.
1. DePalma et al. (2011) 2. Balague et al. (2012) 3. Zhang et al. (2010) 4. Humzah et al. (1988) 5. Ohtori et al. (2015) 6. Yang et al. (2018) 7. Woolf et al. (2010) 8. Chung et al. (2004) 9. Nasto et al. (2013) 10. Yowtak et al. (2011)