Essential role of mitochondrial permeability transition in vanilloid receptor 1-dependent cell death of sensory neurons

Chan Young Shin, Jieun Shin, Byung Moon Kim, Myeong Hyeon Wang, Jung Hee Jang, Young Joon Surh, Uhtaek Oh

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64 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)57-68
Number of pages12
JournalMolecular and Cellular Neuroscience
Issue number1
Publication statusPublished - 2003 Sept 1

Bibliographical note

Funding Information:
This work was supported by Creative Research Initiatives of the Ministry of Science and Technology of Korea and in part by a BK21 program.

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cellular and Molecular Neuroscience
  • Cell Biology


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