Kepler K L, Bodnar R J
Department of Psychology, Queens College, CUNY, Flushing 11367.
Pharmacol Biochem Behav. 1988 Jan;29(1):83-8. doi: 10.1016/0091-3057(88)90278-x.
Continuous cold-water swims (CCWS) elicit a nonopioid and neurohormonal analgesia which displays adaptation. The norepinephrine (NE) system has been implicated since parallel alterations in NE occur following acute and repeated CCWS exposure, and since CCWS analgesia is reduced by locus coeruleus lesions and is potentiated by clonidine and desipramine. The present study evaluated the effects of the alpha-2 NE receptor antagonist, yohimbine upon CCWS (2 degrees C for 3.5 min) analgesia on the jump and tail-flick tests, CCWS hypothermia, and basal nociceptive and thermoregulatory measures in rats. Yohimbine (0.1-2.0 mg/kg, IP) dose-dependently increased basal jump thresholds and potentiated CCWS analgesia: these effects appeared to be additive. Yohimbine potentiated CCWS analgesia on the tail-flick test without altering basal latencies. Yohimbine failed to alter either CCWS hypothermia or basal thermoregulation. Since yohimbine and clonidine, an alpha-2 NE receptor antagonist and agonist respectively, similarly potentiate CCWS analgesia, it appears that NE effects are orthoganol to the intrinsic system mediating CCWS.
持续冷水游泳（CCWS）可引发一种非阿片类神经激素性镇痛，且这种镇痛会出现适应性变化。去甲肾上腺素（NE）系统与CCWS有关，因为在急性和反复暴露于CCWS后，NE会发生平行改变，而且CCWS镇痛会因蓝斑损伤而减弱，并因可乐定和地昔帕明而增强。本研究评估了α-2 NE受体拮抗剂育亨宾对大鼠在跳跃和甩尾试验中CCWS（2℃，持续3.5分钟）镇痛、CCWS体温过低以及基础伤害性感受和体温调节指标的影响。育亨宾（0.1 - 2.0毫克/千克，腹腔注射）剂量依赖性地提高基础跳跃阈值并增强CCWS镇痛：这些作用似乎具有相加性。育亨宾在甩尾试验中增强CCWS镇痛，而不改变基础潜伏期。育亨宾未能改变CCWS体温过低或基础体温调节。由于育亨宾和可乐定分别为α-2 NE受体拮抗剂和激动剂，它们同样增强CCWS镇痛，因此看来NE的作用与介导CCWS的内在系统相互正交。
