ArticleFrontiers in pharmacology2026
Linalyl acetate alleviates inflammatory pain via OLFR482 activation in the mouse anterior cingulate cortex.
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
Introduction: Chronic pain severely impairs quality of life and causes heavy socioeconomic burdens worldwide. Linalyl acetate (LA), a major volatile terpenoid ester from essential oils, possesses potential analgesic effects. Methods: A CFA-induced chronic inflammatory pain mouse model was established. Behavioral tests, immunofluorescence, whole-cell patch-clamp recording, RNA-seq, molecular docking, molecular dynamics simulation and AAV-mediated gene knockdown were applied to explore the analgesic mechanism of LA. Results: Systemic LA administration significantly alleviated inflammatory pain and suppressed neuronal hyperexcitability in the anterior cingulate cortex (ACC). Transcriptome analysis revealed marked upregulation of Olfr482 in the ACC of CFA-treated mice, and molecular docking confirmed the interaction between LA and OLFR482. Olfr482 knockdown largely abolished the analgesic effect of LA. Discussion: LA relieves chronic inflammatory pain via an olfactory-independent mechanism by activating OLFR482 and reducing neuronal hyperexcitability in the ACC. LA is a promising candidate for developing novel analgesic drugs.
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