• Mi Sun Kim, Chul-Kyu Park, Kyu-Young Yeon, Hai Ying Li, Sung Jun Jung, Se-Young Choi, Sung Joong Lee, Kyungpyo Park, Joong Soo Kim, and Seog Bae Oh.
• Department of Physiology and Program in Molecular and Cellular Neuroscience, College of Dentistry and Dental Research Institute, Seoul National University, Seoul, Korea.
• Neuroreport. 2006 Feb 6; 17 (2): 145-9.

AbstractCapsaicin has been used as a topical analgesic to treat diverse pain conditions. We investigated the molecular mechanisms that mediate the inhibition of high-voltage-activated calcium channel currents (ICa) using trigeminal ganglion neurons and a heterologous expression system. Capsaicin inhibited ICa in capsaicin-sensitive trigeminal ganglion neurons, but not in capsaicin-insensitive neurons. Single-cell reverse-transcription polymerase chain reaction revealed the expression of TRPV1 only in capsaicin-sensitive neurons. Capsaicin inhibited ICa in transient receptor potential vanilloid-1-expressing C2D7 cells stably expressing human N-type calcium channels, whereas capsaicin failed to inhibit ICa in naïve C2D7 cells with no endogenous transient receptor potential vanilloid-1 expression. Calcium influx via transient receptor potential vanilloid-1 is not likely to play a critical role in capsaicin-induced ICa inhibition in trigeminal ganglion neurons. ICa inhibition might be one of the mechanisms for the analgesic effect of capsaicin.

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