中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2017, Vol. 12 ›› Issue (6): 981-986.doi: 10.4103/1673-5374.208594

• 原著:颅神经损伤修复保护与再生 • 上一篇    下一篇

轻度闭合性颅脑损伤诱导三叉神经核单胺类神经递质变化：颌面疼痛和头痛的可能机制

  

  • 收稿日期:2017-04-22 出版日期:2017-06-15 发布日期:2017-06-15
  • 基金资助:

    美国退伍军人事务部Merit Review奖(No. B6570R, B78071, and B1005-R)

Mild closed head traumatic brain injury-induced changes in monoamine neurotransmitters in the trigeminal subnuclei of a rat model: mechanisms underlying orofacial allodynias and headache

Golam Mustafa1, 2, Jiamei Hou1, 2, Rachel Nelson1, Shigeharu Tsuda2, Mansura Jahan1, Naweed S. Mohammad1, Joseph V. Watts1, Floyd J. Thompson1, 2, 3, Prodip Bose1, 2, 4   

  1. 1 Brain Rehabilitation Research Center of Excellence, Malcom Randall VA Medical Center, North Florida/South Georgia Veterans Health System, Gainesville, FL, USA; 2 Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL, USA; 3 Department of Neuroscience, McKnight Brain Institute, College of Medicine, University of Florida, Gainesville, FL, USA; 4 Department of Neurology, McKnight Brain Institute, College of Medicine, University of Florida, Gainesville, FL, USA
  • Received:2017-04-22 Online:2017-06-15 Published:2017-06-15
  • Contact: Prodip Bose, M.D., Ph.D., pkbose@ufl.edu or Prodip.bose@va.gov.
  • Supported by:

    This work was supported by Merit Review Awards (No. B6570R, B78071, and B1005-R) from the United States (U.S.) Department of Veterans Affairs Rehabilitation Research and Development Service.

PDF

575

摘要：

最近研究发现，闭合性颅脑损伤啮齿类动物模型表现出渐进性口面触摸痛，一种由非疼痛刺激诱发的高敏痛觉反应，其发生与一些已知的痛觉信号受体和三叉神经痛信号通路分子变化，特别是三叉神经脊束尾核中的变化有关；基于此，实验希望揭示轻度闭合性颅脑损伤大鼠模型中，与触觉性异常疼痛、触摸压力敏感性和内脏痛有关的其他三叉神经核中单胺类神经递质发生了哪些变化。我们发现，三叉神经脊束核吻侧亚核(Sp5O)和极间亚核(Sp5I)中，通常可参与调节触觉和机械刺激敏感性、热敏性的单胺类神经递质5-羟色胺表达发生明显变化；同时，我们还发现孤束核中5-羟色胺和去甲肾上腺素表达发生明显变化，这提示其可能与内脏痛以及与轻度闭合性颅脑损伤孤束核障碍相关的病变有关。这说明，三叉神经核中的单胺类神经递质的变化可能与创伤性脑损伤后颌面疼痛和头痛有关。

ORCID:0000-0000-1378-3644(Prodip Bose)

关键词: 轻度创伤性脑损伤, 三叉神经感觉系统, 神经调质, 面部和躯体触摸痛, 热痛觉过敏, 头痛, 偏头痛

Abstract:

Our recent findings have demonstrated that rodent models of closed head traumatic brain injury exhibit comprehensive evidence of progressive and enduring orofacial allodynias, a hypersensitive pain response induced by non-painful stimulation. These allodynias, tested using thermal hyperalgesia, correlated with changes in several known pain signaling receptors and molecules along the trigeminal pain pathway, especially in the trigeminal nucleus caudalis. This study focused to extend our previous work to investigate the changes in monoamine neurotransmitter immunoreactivity changes in spinal trigeminal nucleus oralis, pars interpolaris and nucleus tractus solitaries following mild to moderate closed head traumatic brain injury, which are related to tactile allodynia, touch-pressure sensitivity, and visceral pain. Our results exhibited significant alterations in the excitatory monoamine, serotonin, in spinal trigeminal nucleus oralis and pars interpolaris which usually modulate tactile and mechanical sensitivity in addition to the thermal sensitivity. Moreover, we also detected a robust alteration in the expression of serotonin, and inhibitory molecule norepinephrine in the nucleus tractus solitaries, which might indicate the possibility of an alteration in visceral pain, and existence of other morbidities related to solitary nucleus dysfunction in this rodent model of mild to moderate closed head traumatic brain injury. Collectively, widespread changes in monoamine neurotransmitter may be related to orofacial allodynhias and headache after traumatic brain injury.

Key words: nerve regeneration, mild to moderate traumatic brain injury, trigeminal sensory system, neuromodulators, facial and somatic allodynia, thermal hyperalgesia, headache, migraine, neural regeneration