Essential role of mitochondrial permeability transition in vanilloid receptor 1-dependent cell death of sensory neurons.
Mol Cell Neurosci
; 24(1): 57-68, 2003 Sep.
Article
en En
| MEDLINE
| ID: mdl-14550768
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.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Dolor
/
Receptores de Droga
/
Capsaicina
/
Mitocondrias
/
Neuronas Aferentes
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Mol Cell Neurosci
Asunto de la revista:
BIOLOGIA MOLECULAR
/
NEUROLOGIA
Año:
2003
Tipo del documento:
Article
País de afiliación:
Corea del Sur