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Nociception

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Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain.

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Related Experiment Video

Updated: Jun 16, 2025

Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities

Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities

Published on: July 29, 2014

Persistent changes in nociceptor translatomes govern hyperalgesic priming in mouse models.

Ishwarya Sankaranarayanan¹, Moeno Kume¹, Ayaan Mohammed¹

¹Pain Neurobiology Research Group, Department of Neuroscience, Center for Advanced Pain Studies, School of Behavioral and Brain Sciences, University of Texas at Dallas, Richardson, Texas.

Biorxiv : the Preprint Server for Biology

|August 16, 2024

Summary

Hyperalgesic priming, a pain sensitization model, is caused by changes in messenger RNA (mRNA) translation within sensory neurons. This study identified specific genes, Gpr88 and Metrn, crucial for this pain plasticity.

Keywords:

GPR88 IL6-mediated hyperalgesic priming Meteorin chemotherapy-induced peripheral neuropathy hyperalgesic priming translating ribosome affinity purification

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Last Updated: Jun 16, 2025

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Area of Science:

Neuroscience
Molecular Biology
Pain Research

Background:

Hyperalgesic priming models plasticity in sensory neurons (nociceptors).
Priming causes normally non-painful stimuli to induce hyperalgesia.
The underlying mechanisms of hyperalgesic priming remain incompletely understood.

Purpose of the Study:

To investigate the hypothesis that hyperalgesic priming results from altered mRNA translation in nociceptors.
To identify specific genes and pathways involved in paclitaxel-induced hyperalgesic priming.

Main Methods:

Utilized paclitaxel as a priming stimulus.
Employed translating ribosome affinity purification (TRAP) sequencing in Nav1.8+ nociceptors.
Analyzed persistent changes in mRNA translation in primed versus control states.

Main Results:

Identified 161 genes with persistently altered mRNA translation following priming.
Found G-protein coupled receptor 88 (Gpr88) mRNA translation upregulated.
Found Meteorin (Metrn) mRNA translation downregulated.

Conclusions:

Altered nociceptor translatomes are causative in producing hyperalgesic priming.
Gpr88 activation exacerbates pain in primed states, while Meteorin reverses priming.
Findings reveal mRNA translation as a key mechanism driving pain sensitization.