Telner J, Lepore F, Guillemot J P
Pharmacol Biochem Behav. 1979 May;10(5):657-61. doi: 10.1016/0091-3057(79)90317-4.
In this study the role of serotonin in pain sensitivity was investigated. Brain serotonin was elevated via low and high doses of precursor tryptophan and lowered via parachlorophenylalanine or lesions placed in the dorsal raphe nucleus. The effects on pain sensitivity were then assessed using two psychophysical pain testing procedures: (1) minimum shock intensity (threshold) which produced a conditioned escape response; and (2) total activity elicited by highly aversive inescapable shock. The results showed that only a large elevation of serotonin produced a change in escape thresholds in the direction of hypoalgesia. When total activity to a painful inescapable stimulus was evaluated only lowering of serotonin produced an effect, and this change was in the direction of hyperalgesia. The conclusion was made that serotonin does contribute to the mechanism of pain.
在本研究中,对血清素在疼痛敏感性中的作用进行了调查。通过低剂量和高剂量的前体色氨酸提高脑内血清素水平,通过对氯苯丙氨酸或损毁中缝背核来降低血清素水平。然后使用两种心理物理学疼痛测试程序评估对疼痛敏感性的影响:(1)产生条件性逃避反应的最小电击强度(阈值);(2)由高度厌恶的不可逃避电击引发的总活动。结果表明,只有血清素大幅升高才会使逃避阈值朝着痛觉减退的方向改变。当评估对疼痛不可逃避刺激的总活动时,只有血清素降低才会产生影响,且这种变化是朝着痛觉过敏的方向。得出的结论是血清素确实参与了疼痛机制。