ArticleFrontiers in pharmacology2026
Suppression of neuropathic pain hypersensitivity by TRPM8 is mediated by mGluR group II and III receptors acting differentially on distinct nociceptor inputs to spinal cord.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Chronic pain following nerve injury (neuropathic pain), is notoriously difficult to treat, with current analgesics showing limited efficacy and adverse or dangerous side effects. One new candidate analgesic target is the TRPM8 ion channel, identified as the peripheral detector for innocuous cool sensation and reported to attenuate spinal cord pain processing by processes involving inhibitory metabotropic glutamate (mGlu) receptors. Methods: Highly selective Group II/III mGluR antagonists and allosteric modulators were used in a nerve injury model to identify the specific receptor subtypes mediating TRPM8-mediated attenuation of nociceptive (pain) processing through peptidergic and non-peptidergic afferent inputs (associated with thermal and mechanical nociception respectively). Integrated experimental approaches involved immunofluorescence histochemistry, functional Ca Results: Differential expression of TRPV1 and MrgprD was demonstrated in peptidergic and non-peptidergic afferents and their selective activation by capsaicin and β-alanine characterised to interrogate transmission at the first central synapses from these afferents in dorsal spinal cord synaptoneurosomes. TRPM8-evoked attenuation of nerve injury-induced increments in capsaicin responses was selectively modified by mGlu Conclusion: Our findings clarify the roles of specific Group II/III mGluRs in the antinociceptive effects of TRPM8 activation against nerve injury-induced hypersensitivity. The mGluRs involved in impacting peptidergic (thermal-associated) nociceptive inputs and non-peptidergic (mechanical-associated) nociceptive inputs appear quite distinct - mGlu
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