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创伤性脑损伤大鼠模型中的伤害性致敏和脑源性神经营养因子上调

Nociceptive sensitization and BDNF up-regulation in a rat model of traumatic brain injury.

作者信息

Feliciano David P, Sahbaie Peyman, Shi Xiaoyou, Klukinov Michael, Clark J David, Yeomans David C

机构信息

Department of Anesthesiology Perioperative and Pain Medicine, 291 Campus Drive, Stanford, CA 94305, United States.

Anesthesiology Service, VA Palo Alto Healthcare System, 3801 Miranda Avenue, Palo Alto, CA 94304, United States.

出版信息

Neurosci Lett. 2014 Nov 7;583:55-9. doi: 10.1016/j.neulet.2014.09.030. Epub 2014 Sep 20.

Abstract

Chronic pain after traumatic brain injury (TBI) is very common, but the mechanisms linking TBI to pain experienced in the periphery have not been described. In this set of studies we examined nociceptive sensitization and changes in spinal cord gene expression using the rat lateral fluid percussion model of mild TBI. We did not identify changes in thermal nociceptive thresholds in rats with mild TBI. However, mechanical allodynia in hind paws contralateral to TBI was significant and sustained. We also found that spinal cord levels of brain derived neurotrophic factor (BDNF) but not several other pain-related genes were up-regulated one week after injury. Our findings suggest that TBI-induced up-regulation of spinal BDNF levels might contribute to chronic TBI-related pain, and that the lateral fluid percussion model might be useful for exploring this relationship.

摘要

创伤性脑损伤(TBI)后的慢性疼痛非常常见,但TBI与外周疼痛之间的联系机制尚未得到描述。在这组研究中,我们使用大鼠轻度TBI的侧方液压冲击模型,研究了伤害性感受敏化和脊髓基因表达的变化。我们未发现轻度TBI大鼠的热痛觉阈值有变化。然而,TBI对侧后爪的机械性异常性疼痛显著且持续存在。我们还发现,损伤后一周,脊髓中脑源性神经营养因子(BDNF)水平上调,但其他几个与疼痛相关的基因未上调。我们的研究结果表明,TBI诱导的脊髓BDNF水平上调可能导致与TBI相关的慢性疼痛,并且侧方液压冲击模型可能有助于探索这种关系。

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