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首页> 外文期刊>BMC Neuroscience >Temporal mismatch between pain behaviour, skin Nerve Growth Factor and intra-epidermal nerve fibre density in trigeminal neuropathic pain
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Temporal mismatch between pain behaviour, skin Nerve Growth Factor and intra-epidermal nerve fibre density in trigeminal neuropathic pain

机译：三叉神经痛中疼痛行为，皮肤神经生长因子和表皮内神经纤维密度之间的时间不匹配

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Background The neurotrophin Nerve Growth factor (NGF) is known to influence the phenotype of mature nociceptors, for example by altering synthesis of neuropeptides, and changes in NGF levels have been implicated in the pathophysiology of chronic pain conditions such as neuropathic pain. We have tested the hypothesis that after partial nerve injury, NGF accumulates within the skin and causes ‘pro-nociceptive’ phenotypic changes in the remaining population of sensory nerve fibres, which could underpin the development of neuropathic pain. Results Eleven days after chronic constriction injury of the rat mental nerve the intra-epidermal nerve fibre density of the chin skin from had reduced from 11.6?±?4.9 fibres/mm to 1.0?±?0.4 fibres/mm; this slowly recovered to 2.4?±?2.0 fibres/mm on day 14 and 4.0?±?0.8 fibres/mm on day 21. Cold hyperalgesia in the ipsilateral lower lip was detectable 11?days after chronic constriction injury, although at this time skin [NGF] did not differ between sides. At 14?days post-injury, there was a significantly greater [NGF] ipsilaterally compared to contralaterally (ipsilateral?=?111?±?23?pg/mg, contralateral?=?69?±?13?pg/mg), but there was no behavioural evidence of neuropathic pain at this time-point. By 21?days post-injury, skin [NGF] was elevated bilaterally and there was a significant increase in the proportion of TrkA-positive (the high-affinity NGF receptor) intra-epidermal nerve fibres that were immunolabelled for the neuropeptide Calcitonin Gene-related peptide. Conclusions The temporal mismatch in behaviour, skin [NGF] and phenotypic changes in sensory nerve fibres indicate that increased [NGF] does not cause hyperalgesia after partial mental nerve injury, although it may contribute to the altered neurochemistry of cutaneous nerve fibres.
机译：背景技术已知神经营养蛋白神经生长因子（NGF）例如通过改变神经肽的合成来影响成熟的伤害感受器的表型，并且NGF水平的变化已经与慢性疼痛状况如神经性疼痛的病理生理有关。我们测试了以下假设：部分神经损伤后，NGF会在皮肤内积累，并在其余感觉神经纤维中引起“伤害感受型”表型改变，这可能会支持神经性疼痛的发展。结果大鼠精神神经慢性压迫损伤后11天，下巴皮肤的表皮内神经纤维密度从11.6±±4.9纤维/ mm降低至1.0±±0.4纤维/ mm。在第14天缓慢恢复至2.4？±？2.0纤维/ mm，在第21天缓慢恢复至4.0？±？0.8纤维/ mm。慢性收缩损伤后11天，同侧下唇出现冷痛觉过敏，尽管此时皮肤双方之间[NGF]没有区别。受伤后第14天，同侧的[NGF]明显高于对侧（同侧的== 111111±？23？pg / mg，对侧的== 69？±？13？pg / mg），但目前尚无神经性疼痛的行为证据。受伤后21天，双侧皮肤[NGF]升高，并且被神经肽降钙素基因-免疫标记的TrkA阳性（高亲和力NGF受体）表皮神经内纤维的比例显着增加。相关肽。结论感觉神经纤维的行为，皮肤[NGF]和表型变化的时间失配表明[NGF]升高虽然会导致皮肤神经纤维的神经化学改变，但并未引起部分精神神经损伤后的痛觉过敏。

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