Secondary traumatic stress increases expression of proteins implicated in peripheral and central sensitization of trigeminal neurons.
Secondary traumatic stress increases expression of proteins implicated in peripheral and central sensitization of trigeminal neurons.
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DOI：
10.1016/j.brainres.2018.03.003
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发表时间：
2018-05-15
期刊：
影响因子：
2.9
通讯作者：
Durham PL
中科院分区：
文献类型：
--
作者：
Hawkins JL;Moore NJ;Miley D;Durham PL
偏头痛是一种常见的神经系统疾病，其病理学涉及三叉神经伤害感受神经元的敏化和激活，以在发作期间促进痛觉过敏和异常性疼痛。偏头痛患者通常表现出神经系统过度兴奋或高度警惕的特征。据报道，三叉神经系统过度兴奋的主要危险因素之一是长期的、无法控制的压力和焦虑。虽然原发性创伤压力是许多疼痛状况的常见风险因素，但在生命早期暴露于继发性创伤压力也被认为是一个促成风险因素。本研究的目的是探讨继发性创伤应激介导的三叉神经脊束核和三叉神经节内细胞的变化。对雄性Sprague道利大鼠（发送者）进行强迫游泳测试（原发性创伤应激），然后将其圈养在与繁殖的雄性和雌性大鼠、妊娠雌性大鼠或雌性大鼠及其哺乳后代（所有接收者）在视觉、嗅觉和听觉上接近的地方。在对二次应激的反应中，与未处理的后代相比，45天的后代三叉神经脊束核中降钙素基因相关肽、有丝分裂原活化蛋白激酶ERK、JNK和p38的活性形式以及胶质细胞酸性蛋白的星形胶质细胞表达水平显著升高。此外，在三叉神经节神经元中观察到ERK和p38的核表达增加。我们的研究结果表明，继发性创伤应激促进与后代三叉神经敏化延长相关的细胞事件，并提供了一种机制，说明早期生活压力可能是偏头痛的危险因素。
The pathology of migraine, a common neurological disease, involves sensitization and activation of trigeminal nociceptive neurons to promote hyperalgesia and allodynia during an attack. Migraineurs often exhibit characteristics of a hyperexcitable or hypervigilant nervous system. One of the primary reported risk factors for development of a hyperexcitable trigeminal system is chronic, unmanaged stress and anxiety. While primary traumatic stress is a commonly cited risk factor for many pain conditions, exposure to secondary traumatic stress early in life is also thought to be a contributing risk factor. The goal of this study was to investigate cellular changes within the spinal trigeminal nucleus and trigeminal ganglion mediated by secondary traumatic stress. Male Sprague Dawley rats (sender) were subjected to forced swim testing (primary traumatic stress) and were then housed in close visual, olfactory, and auditory proximity to the breeding male and female rats, pregnant female rats, or female rats and their nursing offspring (all receivers). In response to secondary stress, levels of calcitonin gene-related peptide, active forms of the mitogen activated protein kinases ERK, JNK, and p38, and astrocyte expression of glial fibrillary acidic protein were significantly elevated in the spinal trigeminal nucleus in day 45 offspring when compared to naïve offspring. In addition, increased nuclear expression of ERK and p38 was observed in trigeminal ganglion neurons. Our results demonstrate that secondary traumatic stress promotes cellular events associated with prolonged trigeminal sensitization in the offspring, and provides a mechanism of how early life stress may function as a risk factor for migraine.
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