Sadowski B
Acta Neurobiol Exp (Wars). 1988;48(1):1-7.
Inbred mouse lines selectively bred for divergent levels of swim induced analgesia were differed in the ability to escape electric footshock. Mice displaying a high analgesia on a hot plate, after swimming for 3 min at 20 degrees centigrade terminated electric current applied at ascending intensity to the grid floor at a higher value compared to the low analgesia line. The difference was particularly pronounced after swim stress, when mice of the former line manifested a serious escape deficit by failing to terminate electric current elikiting apparently aversive phenomena, such as vocalization, runing and jumping. This escape deficit was reserved by naloxone, an opioid antagonist. Results are interpreted in terms of an assumed amnesic effect of endogenous peptides released under the conditions of swim stress. Such interpretation is justified by the data indicating a greater opioid involvement in the swim analgesia in the high analgesia line, compared to low analgesia mice, in which non-opioid mechanisms prevail.
为不同水平的游泳诱导镇痛而选择性培育的近交系小鼠在逃避电击足部刺激的能力上存在差异。在20摄氏度下游泳3分钟后，在热板上表现出高镇痛作用的小鼠，与低镇痛系相比，能在更高的值时终止施加到网格地板上强度逐渐增加的电流。这种差异在游泳应激后尤为明显，此时前一组小鼠表现出严重的逃避缺陷，未能终止引发明显厌恶现象（如发声、奔跑和跳跃）的电流。这种逃避缺陷可被阿片类拮抗剂纳洛酮逆转。结果根据在游泳应激条件下释放的内源性肽的假定失忆作用来解释。与低镇痛小鼠（其中非阿片类机制占主导）相比，表明高镇痛系在游泳镇痛中阿片类物质参与更多的数据证明了这种解释是合理的。
