Logo image
The Nociceptor Primary Cilium Contributes to Mechanical Nociceptive Threshold and Inflammatory and Neuropathic Pain
Journal article   Peer reviewed

The Nociceptor Primary Cilium Contributes to Mechanical Nociceptive Threshold and Inflammatory and Neuropathic Pain

Lindsey A Fitzsimons, Larissa Staurengo-Ferrari, Eugen V Khomula, Oliver Bogen, Dionéia Araldi, Ivan J M Bonet, Paul G Green, Ethan E Jordan, Finn Sclafani, Connor E Nowak, …
The Journal of neuroscience, Vol.44(47), p.e1265242024
11/20/2024
DOI: 10.1523/JNEUROSCI.1265-24.2024
PMID: 39349056

View Online

Abstract

The primary cilium, a single microtubule-based organelle protruding from the cell surface and critical for neural development, also functions in adult neurons. While some dorsal root ganglion neurons elaborate a primary cilium, whether it is expressed by and functional in nociceptors is unknown. Recent studies have shown the role of Hedgehog, whose canonical signaling is primary cilium dependent, in nociceptor sensitization. We establish the presence of primary cilia in soma of rat nociceptors, where they contribute to mechanical threshold, prostaglandin E (PGE )-induced hyperalgesia, and chemotherapy-induced neuropathic pain (CIPN). Intrathecal administration of siRNA targeting , a primary cilium-specific intraflagellar transport (IFT) protein required for ciliary integrity, resulted in attenuation of mRNA and nociceptor primary cilia. Attenuation of primary cilia was associated with an increase in mechanical nociceptive threshold in vivo and decrease in nociceptor excitability in vitro, abrogation of hyperalgesia, and nociceptor sensitization induced by both a prototypical pronociceptive inflammatory mediator PGE and paclitaxel CIPN, in a sex-specific fashion. siRNA targeting , another IFT protein, and knockdown of NompB, the ortholog, also abrogated CIPN and reduced baseline mechanosensitivity, respectively, providing independent confirmation for primary cilia control of nociceptor function. Hedgehog-induced hyperalgesia is attenuated by siRNA, supporting the role for primary cilia in Hedgehog-induced hyperalgesia. Attenuation of CIPN by cyclopamine (intradermal and intraganglion), which inhibits Hedgehog signaling, supports the role of Hedgehog in CIPN. Our findings support the role of the nociceptor primary cilium in control of mechanical nociceptive threshold and inflammatory and neuropathic pain, the latter Hedgehog-dependent.
Animals Cilia - metabolism Dinoprostone - metabolism Dinoprostone - pharmacology Female Ganglia, Spinal - metabolism Hedgehog Proteins - genetics Hedgehog Proteins - metabolism Hyperalgesia - chemically induced Hyperalgesia - metabolism Hyperalgesia - physiopathology Inflammation - chemically induced Inflammation - metabolism Male Neuralgia - metabolism Neuralgia - physiopathology Nociceptors - metabolism Paclitaxel - pharmacology Pain Threshold - physiology Rats Rats, Sprague-Dawley

Details

Logo image