Modulation of oral heat and cold pain by irritant chemicals
Modulation of oral heat and cold pain by irritant chemicals
复制标题
DOI：
10.1093/chemse/bjm056
复制
发表时间：
2008-01-01
期刊：
影响因子：
3.5
通讯作者：
Carstens, E.
中科院分区：
文献类型：
--
作者：
Albin, Kelly C.;Carstens, Mirela Iodi;Carstens, E.
常见的食物刺激物通过作用于温度敏感的瞬时感受器电位(Trp)通道而引起口腔热感或冷感。我们使用半舌、两种选择的强迫选择程序，结合双侧疼痛强度等级来研究对热痛和冷痛的刺激性影响。该方法在双边温差检测任务中得到了验证。辣椒素、芥子油和肉桂醛增加了49摄氏度刺激引起的舌热疼痛。芥子油和肉桂醛对舌冷痛(9.5摄氏度)有微弱的增强作用，而辣椒素则没有作用。薄荷醇可显著增强冷痛，但对热痛有微弱的缓解作用。为了说明辣椒素的作用是否归因于感知上相似的热和化学感觉的总和，应用辣椒素使一半的舌头脱敏。重新应用辣椒素后，辣椒素几乎或没有引起刺激性感觉，但仍显著增加了辣椒素治疗侧的热痛，排除了总和的可能性。在第三个实验中，辣椒素显著提高了对分级热刺激(47摄氏度至50摄氏度)的疼痛评级，导致刺激反应功能向上移动。薄荷醇可通过增强外周纤维中TRPM8的热门效应而诱导冷痛敏。辣椒素、芥子油和肉桂糖苷可通过增强与外周伤害性感受器中的TRPA1共表达的TRPV1的热门来诱导热痛觉过敏。
Common food irritants elicit oral heat or cool sensations via actions at thermosensitive transient receptor potential (TRP) channels. We used a half-tongue, 2-alternative forced-choice procedure coupled with bilateral pain intensity ratings to investigate irritant effects on heat and cold pain. The method was validated in a bilateral thermal difference detection task. Capsaicin, mustard oil, and cinnamaldehyde enhanced lingual heat pain elicited by a 49 degrees C stimulus. Mustard oil and cinnamaldehyde weakly enhanced lingual cold pain (9.5 degrees C), whereas capsaicin had no effect. Menthol significantly enhanced cold pain and weakly reduced heat pain. To address if capsaicin's effect was due to summation of perceptually similar thermal and chemical sensations, one-half of the tongue was desensitized by application of capsaicin. Upon reapplication, capsaicin elicited little or no irritant sensation yet still significantly enhanced heat pain on the capsaicin-treated side, ruling out summation. In a third experiment, capsaicin significantly enhanced pain ratings to graded heat stimuli (47 degrees C to 50 degrees C) resulting in an upward shift of the stimulus-response function. Menthol may induce cold hyperalgesia via enhanced thermal gating of TRPM8 in peripheral fibers. Capsaicin, mustard oil, and cinnanamdelyde may induce heat hyperalgesia via enhanced thermal gating of TRPV1 that is coexpressed with TRPA1 in peripheral nociceptors.