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首页> 美国卫生研究院文献>Brain >Priming of adult pain responses by neonatal pain experience: maintenance by central neuroimmune activity
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Priming of adult pain responses by neonatal pain experience: maintenance by central neuroimmune activity

机译：通过新生儿疼痛经验引发成人疼痛反应：通过中枢神经免疫活性维持

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摘要

Adult brain connectivity is shaped by the balance of sensory inputs in early life. In the case of pain pathways, it is less clear whether nociceptive inputs in infancy can have a lasting influence upon central pain processing and adult pain sensitivity. Here, we show that adult pain responses in the rat are ‘primed’ by tissue injury in the neonatal period. Rats that experience hind-paw incision injury at 3 days of age, display an increased magnitude and duration of hyperalgesia following incision in adulthood when compared with those with no early life pain experience. This priming of spinal reflex sensitivity was measured by both reductions in behavioural withdrawal thresholds and increased flexor muscle electromyographic responses to graded suprathreshold hind-paw stimuli in the 4 weeks following adult incision. Prior neonatal injury also ‘primed’ the spinal microglial response to adult injury, resulting in an increased intensity, spatial distribution and duration of ionized calcium-binding adaptor molecule-1-positive microglial reactivity in the dorsal horn. Intrathecal minocycline at the time of adult injury selectively prevented both the hyperalgesia and early microglial reactivity associated with prior neonatal injury. The enhanced neuroimmune response seen in neonatally primed animals could also be demonstrated in the absence of peripheral tissue injury by direct electrical stimulation of tibial nerve fibres, confirming that centrally mediated mechanisms contribute to these long-term effects. These data suggest that early life injury may predispose individuals to enhanced sensitivity to painful events.
机译：成人大脑的连通性是由早期生活中感觉输入的平衡所决定的。就疼痛途径而言，尚不清楚婴儿期的伤害性输入能否对中枢性疼痛的产生和成人疼痛的敏感性产生持久影响。在这里，我们表明，新生阶段大鼠的成年疼痛反应是由组织损伤引起的。与没有早期疼痛经历的大鼠相比，在3天大时遭受后爪切口损伤的大鼠在成年后切口表现出增加的痛觉过敏的幅度和持续时间。脊柱反射敏感性的这种启动是通过在成年切口后4周内行为退缩阈值的降低和屈肌肌电肌对分级超阈后爪刺激的增强反应来衡量的。先前的新生儿损伤也“引发”了对成年损伤的脊髓小胶质细胞反应，导致背角中离子钙结合衔接子分子1阳性小胶质细胞反应性的强度，空间分布和持续时间增加。成人损伤时鞘内注射米诺环素选择性预防痛觉过敏和与先前新生儿损伤相关的早期小胶质细胞反应。通过直接电刺激胫神经纤维，在没有周围组织损伤的情况下，也可以证明在新生动物身上看到的增强的神经免疫反应，这证实了中央介导的机制有助于这些长期作用。这些数据表明，生命早期伤害可能使个体对疼痛事件的敏感性增强。

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