Lichtman Aron H, Smith Forrest L, Martin Billy R
Department of Pharmacology and Toxicology, MCV Station, Medical College of Virginia / Virginia Commonwealth University, Richmond, VA 23298 USA.
Pain. 1993 Dec;55(3):283-295. doi: 10.1016/0304-3959(93)90003-8.
It has recently been hypothesized that tail-skin temperature may exert a profound influence on the latency of the tail-flick response to radiant heat. Several recent reports in the literature urge investigators to assess tail temperatures concurrently when using the tail-flick test and to adjust the tail-flick latency by a coefficient when a change in tail temperature is detected. Because much of the supporting evidence of this hypothesis was strictly correlational, the purpose of the present study was to determine whether tail-skin temperature is an important factor contributing to the latency of the tail-flick response to radiant heat. The effects of a series of pharmacological and non-pharmacological manipulations on tail-skin temperature and response latencies were assessed using either a low-intensity or high-intensity tail-flick stimulus. In addition, colonic temperature was evaluated. None of the drug treatments yielded a significant correlation between tail temperature and tail-flick latency. Of the seven drugs tested, only mecamylamine produced a consistent change in tail-skin temperature. Although mecamylamine significantly elevated tail temperature by more than 2 degrees C, it failed to alter response latencies. Similarly tail submergence into 5 degrees C water for 10 sec led to profound decreases in tail temperature ranging from -6.5 to -7.6 degrees C while producing only minimal increases in tail-flick latency. Conversely, submerging the tail in 38 degrees C water or placing the animals over a heating pad maintained at 38 degrees C increased tail temperatures at least 2 degrees C without affecting response latencies. Inverse correlations were found between tail-flick latency and colonic temperature after morphine, delta 9-tetrahydrocannabinal (delta 9-THC), and nicotine administration; however, these relationships do not appear to be causal. Sodium barbital produced far more hypothermia than any other agent, but did not produce any antinociception. Moreover, placing subjects in heated cages increased tail-skin temperature between 2 and 4 degrees C and blocked the hypothermic effects of morphine and delta 9-THC without reducing the antinociceptive potencies of these agents. These findings indicate that tail-skin and core temperatures have a negligible influence on the tail-flick response. We conclude that monitoring tail-skin or core temperatures when employing the tail-flick test is unnecessary and altering tail-flick latencies to account for changes in tail temperature is unwarranted.
最近有人提出假说,认为尾皮温度可能对辐射热引起的甩尾反应潜伏期产生深远影响。文献中最近的几份报告敦促研究人员在使用甩尾试验时同时评估尾温,并在检测到尾温变化时通过系数调整甩尾潜伏期。由于该假说的许多支持证据严格来说都是相关性的,因此本研究的目的是确定尾皮温度是否是导致辐射热引起的甩尾反应潜伏期的一个重要因素。使用低强度或高强度甩尾刺激评估了一系列药理和非药理操作对尾皮温度和反应潜伏期的影响。此外,还评估了结肠温度。没有一种药物治疗能使尾温与甩尾潜伏期之间产生显著相关性。在所测试的七种药物中,只有美加明能使尾皮温度产生持续变化。虽然美加明使尾温显著升高超过2摄氏度,但它未能改变反应潜伏期。同样,将尾巴浸入5摄氏度的水中10秒会导致尾温大幅下降,范围在-6.5至-7.6摄氏度之间,而甩尾潜伏期仅略有增加。相反,将尾巴浸入38摄氏度的水中或把动物放在保持在38摄氏度的加热垫上会使尾温至少升高2摄氏度,而不影响反应潜伏期。在给予吗啡、Δ9-四氢大麻酚(Δ9-THC)和尼古丁后,发现甩尾潜伏期与结肠温度呈负相关;然而,这些关系似乎并非因果关系。戊巴比妥钠产生的体温过低比任何其他药物都严重,但没有产生任何镇痛作用。此外,将实验对象置于加热笼中可使尾皮温度升高2至4摄氏度,并阻断吗啡和Δ9-THC的体温过低效应,而不降低这些药物的镇痛效力。这些发现表明,尾皮温度和核心温度对甩尾反应的影响可以忽略不计。我们得出结论,在进行甩尾试验时监测尾皮温度或核心温度是不必要的,并且为了考虑尾温变化而改变甩尾潜伏期是没有根据的。