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海湾战争药剂溴吡斯的明和氯菊酯引起超敏性伤害感受,这种伤害感受在迷走神经刺激后得到恢复。

Gulf War agents pyridostigmine bromide and permethrin cause hypersensitive nociception that is restored after vagus nerve stimulation.

机构信息

Department of Neuroscience and Experimental Therapeutics, Texas A&M University Health Science Center, United States.

Dept. of Biomedical Sciences, Burrell College of Osteopathic Medicine, Las Cruces, NM 88001.

出版信息

Neurotoxicology. 2018 Dec;69:93-96. doi: 10.1016/j.neuro.2018.09.007. Epub 2018 Sep 29.

DOI:10.1016/j.neuro.2018.09.007
PMID:30273628
Abstract

Gulf war illness (GWI) is a chronic multi-symptom disease that afflicts 25-33% of troops that were deployed in the 1990-1991 Gulf War. GWI symptoms include cognitive, behavioral and emotional deficits, as well as migraines and pain. It is possible that exposure to Gulf War agents and prophylactics contributed to the reported symptomology. Pyridostigmine bromide (PB) and permethrin (PER) were given to protect from nerve gas attacks and insect vector born disease, respectively. Previous studies have demonstrated that 10 days of exposure to these chemicals can cause symptoms analogous to those observed in GWI, including impairment of long-term memory in mice. Other studies using this model have shown chronic neuroinflammation, and chronic neuroinflammation can lead to altered nociceptive sensitivity. At 10-weeks after the 10-day PB and PER exposure paradigm, we observed lowered nociceptive threshold on the Von Frey test that was no longer evident at 28 weeks and 38 weeks post-exposure. We further determined that vagus nerve stimulation, initiated at 38 weeks after exposure, restores the lowered nociceptive sensitivity. Therefore, stimulating the vagus nerve appears to influence nociception. Future studies are need to elucidate possible mechanisms of this effect.

摘要

海湾战争病(GWI)是一种慢性多症状疾病,影响了 1990-1991 年海湾战争中部署的 25-33%的部队。GWI 的症状包括认知、行为和情绪缺陷,以及偏头痛和疼痛。海湾战争制剂和预防性药物的暴露可能导致了报告的症状。派姆溴铵(PB)和氯菊酯(PER)分别用于防止神经毒气袭击和昆虫媒介传播疾病。先前的研究表明,暴露于这些化学物质 10 天可引起类似于 GWI 中观察到的症状,包括小鼠的长期记忆受损。使用该模型的其他研究表明,慢性神经炎症会导致痛觉敏感性改变。在 PB 和 PER 暴露 10 天后的 10 周,我们观察到 Von Frey 测试中的痛觉阈值降低,而在暴露后 28 周和 38 周时不再明显。我们进一步确定,在暴露后 38 周开始刺激迷走神经可恢复降低的痛觉敏感性。因此,刺激迷走神经似乎会影响痛觉。需要进一步的研究来阐明这种影响的可能机制。

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