Liu L, Simon S A
Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA.
Neurosci Lett. 1997 May 30;228(1):29-32. doi: 10.1016/s0304-3940(97)00358-3.
Vanilloid receptors are activated by capsaicin, the pungent ingredient in hot pepper. They are also specifically and competitively inhibited by capsazepine (CPZ). To determine whether CPZ is specific to vanilloid receptors, its effects were tested on the currents evoked by nicotine in rat trigeminal ganglia. We found that 10 microM CPZ, a concentration frequently used to inhibit capsaicin's physiological responses attributed to capsaicin, reversibly inhibits (40%) the magnitude of the currents activated by 100 microM nicotine. We conclude that 10 microM capsazepine can alter the effects of channels other than those activated by capsaicin, and thus caution must be used in attributing all the CPZ-sensitive physiological effects to those only produced by blocking of vanilloid receptors.
香草酸受体可被辣椒素激活，辣椒素是辣椒中的辛辣成分。它们也会被辣椒平（CPZ）特异性且竞争性地抑制。为了确定CPZ是否对香草酸受体具有特异性，研究人员测试了其对大鼠三叉神经节中尼古丁诱发电流的影响。我们发现，10微摩尔CPZ（一种常用于抑制归因于辣椒素的生理反应的浓度）可可逆地抑制（40%）由100微摩尔尼古丁激活的电流大小。我们得出结论，10微摩尔辣椒平可改变除辣椒素激活的通道以外的其他通道的作用，因此在将所有对CPZ敏感的生理效应都归因于仅通过阻断香草酸受体产生的效应时必须谨慎。
