Sternberg W F, Liebeskind J C
Department of Psychology, University of California, Los Angeles 90005-1563, USA.
Eur J Anaesthesiol Suppl. 1995 May;10:14-7.
The brain contains neuronal circuits, activation of which by electrical stimulation or environmental stress causes analgesia. Both opioid and non-opioid forms of stimulus-induced analgesia exist, and are anatomically differentiated. Several transmitters have been postulated for non-opioid stimulus-induced analgesia, N-methyl-D-aspartic acid being a particularly likely candidate. In mice there are marked gender differences in the underlying neurochemical medication of stress-induced analgesia, the development of which is sensitive to the hormonal environment during early post-natal development and which changes with age in both sexes. Mice can be bred for a high or low analgesic response to stress and there is evidence that this is determined by a single gene. Operative pain, as a stressor, inhibits natural killer (NK) cell activity and influences the propensity to develop metastases when mice are inoculated with an experimental tumour after abdominal surgery. This can be influenced by peri-operative morphine in analgesic doses.
大脑包含神经元回路，通过电刺激或环境应激激活这些回路会产生镇痛作用。刺激诱导的镇痛作用存在阿片类和非阿片类两种形式，且在解剖学上有所区分。对于非阿片类刺激诱导的镇痛作用，已经提出了几种神经递质，其中N-甲基-D-天冬氨酸是一个特别有可能的候选者。在小鼠中，应激诱导镇痛的潜在神经化学调节存在明显的性别差异，其发展对出生后早期发育期间的激素环境敏感，并且在两性中都会随年龄而变化。可以培育出对应激产生高镇痛反应或低镇痛反应的小鼠，有证据表明这是由单个基因决定的。手术疼痛作为一种应激源，会抑制自然杀伤（NK）细胞的活性，并在小鼠腹部手术后接种实验性肿瘤时影响发生转移的倾向。这可以受到镇痛剂量的围手术期吗啡的影响。
