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首页> 外文期刊>Behavioral neuroscience >Pain Chronification and Chronic Pain Impair a Defensive Behavior, But Not the Ability of Acute Pain to Facilitate It, Through the Activation of an Endogenous Analgesia Circuit
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Pain Chronification and Chronic Pain Impair a Defensive Behavior, But Not the Ability of Acute Pain to Facilitate It, Through the Activation of an Endogenous Analgesia Circuit

机译:疼痛计数和慢性疼痛损害防御性行为,但不能通过激活内源性镇痛回路来促进它的急性疼痛的能力

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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 mu-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.
机译:在危及生命的情况下减少疼痛感知的内源性能力对于预防恢复行为来说是至关重要的,并使受试者自由地从事适当的防御反应。我们之前已经表明,急性疼痛激活上升的伤害 - 一种内源性镇痛电路,依赖于细胞核内的阿片类药物 - 以促进滋补不动响应,是一种先天的防守行为。现在,我们询问慢性疼痛和疼痛计数是否损害了滋补不动响应或急性疼痛的能力,通过激活升高的伤害控制来促进它。我们发现在持久性机械痛觉术期间大鼠的滋补不动响应持续时间持续时间显着降低。这一发现表明,慢性痛苦及其发展损害防守响应。然而,在持续痛觉过敏的诱导和维持阶段期间,通过前烷胶囊注射的升高的伤害性对照激活,增加了滋补不动响应,通过核心内骨膜内的u-Fomioid受体阻断的效果。该发现表明,疼痛计时和慢性疼痛不会阻止急性疼痛的能力,以促进滋补不动的防御性行为通过激活上升的伤害控制。因此,虽然慢性痛苦状态降低了从事防守行为的能力,但它们可能不会阻止在威胁危及危及急性疼痛的情况下表达防守行为。这种机制的生物学目的可能是在新的危及危及危及危及局部的情况下增加受伤对象的存活率。

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