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• W2014014048 abstract "Capsaicin causes pain by activating VR1, a cloned capsaicin receptor, in sensory neurons. After the initial excitatory responses, capsaicin produces prolonged analgesia, presumably because of the neurotoxic effect that leads to the death of sensory neurons. However, the mechanism underlying capsaicin-induced cell death of sensory neurons is not known. Here we report that capsaicin induces cell death in VR1-expressing sensory neurons and VR1-transfected human embryonic kidney cells. Cell death of sensory neurons induced by capsaicin is accompanied by DNA fragmentation, TUNEL staining, and shrinkage of the nucleus in a caspase-dependent manner, indicating the apoptotic nature of the cell death. Mitochondrial permeability transition is likely to be a major component of capsaicin-induced cell death because bonkrekic acid and cyclosporin A, inhibitors of mitochondrial permeability transition, block this cell death. These results imply that capsaicin induces mitochondrial dysfunction in VR1-expressing cells, leading to apoptotic cell death, which is a well-known neurotoxic effect of capsaicin." @default.
• W2014014048 created "2016-06-24" @default.
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• W2014014048 date "2003-09-01" @default.
• W2014014048 modified "2023-10-11" @default.
• W2014014048 title "Essential role of mitochondrial permeability transition in vanilloid receptor 1-dependent cell death of sensory neurons" @default.
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• W2014014048 doi "https://doi.org/10.1016/s1044-7431(03)00121-0" @default.
• W2014014048 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14550768" @default.
• W2014014048 hasPublicationYear "2003" @default.
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