Sex differences in mechanisms of pain hypersensitivity

Mogil, Jeffrey S.; Parisien, Marc; Esfahani, Sahel J.; Diatchenko, Luda

doi:10.1016/j.neubiorev.2024.105749

Neuroscience & Biobehavioral Reviews

2024

DOI: 10.1016/j.neubiorev.2024.105749

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Sex differences in mechanisms of pain hypersensitivity

Jeffrey S. Mogil,

Marc Parisien,

Sahel J. Esfahani

et al.

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2024

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References 220 publications

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Persistent changes in nociceptor translatomes govern hyperalgesic priming in mouse models

Sankaranarayanan,

Kume,

Mohammed

et al. 2024

Preprint

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Hyperalgesic priming is a model system that has been widely used to understand plasticity in painful stimulus-detecting sensory neurons, called nociceptors. A key feature of this model system is that following priming, stimuli that do not normally cause hyperalgesia now readily provoke this state. We hypothesized that hyperalgesic priming occurs due to reorganization of translation of mRNA in nociceptors. To test this hypothesis, we used paclitaxel treatment as the priming stimulus and translating ribosome affinity purification (TRAP) to measure persistent changes in mRNA translation in Nav1.8+ nociceptors. TRAP sequencing revealed 161 genes with persistently altered mRNA translation in the primed state. We identifiedGpr88as upregulated andMetrnas downregulated. We confirmed a functional role for these genes, wherein a GPR88 agonist causes pain only in primed mice and established hyperalgesic priming is reversed by Meteorin. Our work demonstrates that altered nociceptor translatomes are causative in producing hyperalgesic priming.

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Persistent changes in nociceptor translatomes govern hyperalgesic priming in mouse models

Sankaranarayanan,

Kume,

Mohammed

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

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Sex differences in mechanisms of pain hypersensitivity

Cited by 1 publication

References 220 publications

Persistent changes in nociceptor translatomes govern hyperalgesic priming in mouse models

Persistent changes in nociceptor translatomes govern hyperalgesic priming in mouse models

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