ArticleThe Korean journal of pain2026
Voltage-gated sodium channel 1.8 contributes to hyperalgesia induced by the coexistence of anxiety and remifentanil exposure.
Article in The Korean journal of pain, 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: Remifentanil-induced hyperalgesia (RIH) is directly mediated by altered mitochondrial dynamics. Moreover, anxiety is proven to worsen hyperalgesia. Voltage-gated sodium channel 1.8 (NaV1.8) is involved in both nociceptive initiation and anxiety. However, its role in modulating RIH, particularly in the coexistence of anxiety and RIH (CARIH), remains unexplored. Methods: A total of 148 Sprague-Dawley male rats were used to explore whether silencing NaV1.8 activation could alleviate CARIH. The behavioral effects were assessed using the open field, novelty suppressed feeding, and paw withdrawal tests. The mechanisms of antisense oligodeoxynucleotides (AS-ODN) targeting NaV1.8 (AS-NaV1.8) were investigated through western blot, RT-qPCR, electron microscopy, mitochondrial superoxide imaging, glutathione (GSH/GSSG) ratio, and malondialdehyde measurement. Results: NaV1.8 was upregulated at the mRNA level in the dorsal root ganglia (DRG) ( Conclusions: Anxiety exacerbates RIH, while NaV1.8 knockdown in DRG effectively attenuates CARIH by suppressing abnormal mitochondrial dynamics. Oral NaV1.8 inhibitors show promise in preclinical trials, suggesting NaV1.8 targeting as a novel approach to mitigate CARIH.
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