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压迫性损伤后痉挛大鼠脊髓中强啡肽A(1-17)含量降低。

Decreased dynorphin A (1-17) in the spinal cord of spastic rats after the compressive injury.

作者信息

Dong Hong-Wei, Wang Li-Hua, Zhang Min, Han Ji-Sheng

机构信息

Neuroscience Research Institute and Department of Neurobiology, Peking University Health Science Center, Beijing 100083, China.

出版信息

Brain Res Bull. 2005 Oct 15;67(3):189-95. doi: 10.1016/j.brainresbull.2005.06.026.

Abstract

Spasticity in rat hindlimbs was induced by compressing cervical spinal cord with a wax ball. Ashworth score and H-reflex were measured 1 week after the surgery. The results showed that: (1) muscle spasm was detected in the hindlimbs a week after the operation and maintained at least 8 weeks, (2) in the spastic animals, dynorphin A (1-17)-ir decreased significantly in thoracic and lumbar segments of the spinal cord and (3) peripheral administration of kappa receptor agonist U50488H and electrical stimulation at 100 Hz effectively relieved the muscle spasm. Our data supported the note that the reduction of endogenous dynorphin A (1-17) might play an important role in the pathogenesis of spinally induced muscle spasticity and the replenishment of its shortage might relieve the spasticity.

摘要

用蜡球压迫大鼠颈脊髓诱导其后肢痉挛。术后1周测量Ashworth评分和H反射。结果显示:(1)术后1周在后肢检测到肌肉痉挛,并持续至少8周;(2)在痉挛动物中,脊髓胸段和腰段强啡肽A(1-17)免疫反应性显著降低;(3)外周给予κ受体激动剂U50488H和100Hz电刺激可有效缓解肌肉痉挛。我们的数据支持这样的观点,即内源性强啡肽A(1-17)的减少可能在脊髓性肌肉痉挛的发病机制中起重要作用,补充其不足可能缓解痉挛。

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