Nociceptive responses to high and low rates of noxious cutaneous heating are mediated by different nociceptors in the rat: Electrophysiological evidence
Nociceptive responses to high and low rates of noxious cutaneous heating are mediated by different nociceptors in the rat: Electrophysiological evidence
复制标题
DOI：
10.1016/s0304-3959(96)03177-6
复制
发表时间：
1996-11-01
期刊：
影响因子：
7.4
通讯作者：
Proudfit, HK
中科院分区：
文献类型：
--
作者：
Yeomans, DC;Proudfit, HK
较高的有害辐射加热率诱发的行为伤害感受反应似乎是由A δ伤害感受受体激活介导的，而较低的皮肤加热率诱发的行为伤害感受反应似乎是由c纤维伤害感受受体激活介导的。从戊巴比妥麻醉大鼠隐神经中分离的A δ和C伤害性传入纤维的单单位记录结果证实了这一假设。在刺激开始后的2秒内，以6.5℃/秒的相对高速率加热大鼠后爪皮肤，激活了a δ单位。这种反应潜伏期与对类似刺激的足部退缩反应的2.5秒潜伏期相似。相比之下，C-纤维在5-6秒的较长潜伏期下仅被轻微激活。相反，以相对较低的0.9℃/秒的速度加热后爪皮肤，激活了C-纤维，但仅激发了少量a δ伤害感受器的动作电位。在加热开始后的8 - 10秒内，c -纤维开始以低于1hz的速率放电，在10 - 12秒内以平均1.5 Hz的速率放电，这与足部退缩反应的潜伏期相对应。辣椒素局部应用于后爪皮肤后，c -纤维反应的潜伏期从8-12秒的控制值减少到大约4秒。在辣椒素治疗后，足部对皮肤加热反应的平均潜伏期也从12-14秒的控制值减少到4-5秒。相比之下，辣椒素治疗并没有显著影响A δ伤害感受器的反应。这些结果支持了以下结论：对低皮肤加热率的痛觉足戒断反应主要是由c纤维痛觉感受器的激活介导的。这些结果提供了直接证据，在这些实验条件下，高皮肤加热率引起的伤害性足部戒断反应主要是由A δ伤害感受器介导的，而低皮肤加热率引起的足部戒断反应主要是由c纤维伤害感受器介导的。
Behavioral nociceptive responses evoked by relatively high rates of noxious radiant skin heating appear to be mediated by A delta nociceptor activation, whereas responses evoked by low rates of skin heating appear to be mediated by the activation of C-fiber nociceptors. This hypothesis was confirmed by the results of single unit recordings of A delta and C nociceptive afferent fibers isolated from the saphenous nerves of pentobarbital anesthetized rats. Heating the hind paw skin of the rat at a relatively high rate of 6.5 degrees C/sec activated A delta units within 2 sec after the onset of the stimulus. This response latency is similar to the 2.5 sec latency of the foot withdrawal response to a similar stimulus. In contrast, C-fibers were only slightly activated at a longer latency of 5-6 sec. Conversely, heating the hind paw skin at a relatively low rate of 0.9 degrees C/sec activated C-fibers, but evoked only a few action potentials in A delta nociceptors. C-fibers began firing at a rate less than 1 Hz between 8 and 10 sec after the onset of heating and fired at a mean rate of 1.5 Hz between 10 and 12 sec, which corresponds to the latency of the foot withdrawal response. Topical application of capsaicin to the hind paw skin decreased the latency of C-fiber responses from control values of 8-12 sec to approximately 4 sec after topical capsaicin treatment. The mean latency of the foot withdrawal response to skin heating at the low rate is also reduced from control values of 12-14 sec to 4-5 sec after capsaicin treatment. In contrast, capsaicin treatment did not significantly affect the responses of A delta nociceptors. These results support the conclusion that nociceptive foot withdrawal responses to a low rate of skin heating are mediated predominantly by the activation of C-fiber nociceptors. These results provide direct evidence that, under the conditions of these experiments, nociceptive foot withdrawal responses evoked by high rates of skin heating are primarily mediated by A delta nociceptors, and foot withdrawal responses evoked by low rates of skin heating are primarily mediated by C-fiber nociceptors.