Lamana Monaliza Simone, Miranda Josiane, Tobaldini Gláucia, Fischer Luana, Tambeli Cláudia Herrera
Department of Physiology, Piracicaba Dental School, State University of Campinas.
Department of Physiology, Division of Biological Sciences, Federal University of Parana.
Behav Neurosci. 2018 Dec;132(6):614-623. doi: 10.1037/bne0000255. Epub 2018 Oct 4.
The endogenous ability to decrease pain perception during life-threatening situations is crucial to the prevention of recuperative behaviors and to leave the subject free to engage in appropriated defensive responses. We have previously shown that acute pain activates the ascending nociceptive control-an endogenous analgesia circuit dependent on opioid mechanisms within nucleus accumbens-to facilitate the tonic immobility response, an innate defensive behavior. Now we asked whether chronic pain and pain chronification impairs either the tonic immobility response or the ability of acute pain to facilitate it by activating the ascending nociceptive control. We found a significant decrease in the duration of the tonic immobility response in rats during the induction and maintenance phases of the persistent mechanical hyperalgesia. This finding suggests that chronic pain and its development impair defensive responses. However, during the induction and maintenance phases of persistent hyperalgesia, the ascending nociceptive control activation, by a forepaw capsaicin injection, increased the tonic immobility response, an effect prevented by the blockade of μ-opioid receptors within nucleus accumbens. This finding suggests that pain chronification and chronic pain do not prevent the ability of acute pain to facilitate the defensive behavior of tonic immobility by activating the ascending nociceptive control. Therefore, although chronic pain states decrease the ability to engage in a defensive behavior, they may not prevent the expression of defensive behaviors during life-threatening situations accompanied by acute pain. The biological purpose of such a mechanism may be to increase the chances of survival of a wounded subject exposed to acute pain in a novel life-threatening situation. (PsycINFO Database Record (c) 2018 APA, all rights reserved).
在危及生命的情况下降低疼痛感知的内源性能力对于预防恢复行为以及使个体能够自由地进行适当的防御反应至关重要。我们之前已经表明,急性疼痛会激活上行伤害性控制——一种依赖伏隔核内阿片类机制的内源性镇痛回路——以促进强直性不动反应,这是一种先天性防御行为。现在我们想知道慢性疼痛和疼痛慢性化是否会损害强直性不动反应,或者急性疼痛通过激活上行伤害性控制来促进该反应的能力。我们发现,在持续性机械性痛觉过敏的诱导和维持阶段,大鼠的强直性不动反应持续时间显著缩短。这一发现表明慢性疼痛及其发展会损害防御反应。然而,在持续性痛觉过敏的诱导和维持阶段,通过前爪注射辣椒素激活上行伤害性控制,会增加强直性不动反应,而这种效应可被伏隔核内μ-阿片受体的阻断所阻止。这一发现表明,疼痛慢性化和慢性疼痛并不会阻止急性疼痛通过激活上行伤害性控制来促进强直性不动这种防御行为的能力。因此,尽管慢性疼痛状态会降低进行防御行为的能力,但它们可能不会阻止在伴有急性疼痛的危及生命的情况下防御行为的表现。这种机制的生物学目的可能是增加在新的危及生命的情况下遭受急性疼痛的受伤个体的生存几率。(PsycINFO数据库记录(c)2018美国心理学会,保留所有权利)