Spinal plasticity following intermittent hypoxia: implications for spinal injury.

Spinal plasticity following intermittent hypoxia: implications for spinal injury.
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DOI:
10.1111/j.1749-6632.2010.05499.x
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发表时间:
2010-06
影响因子:
5.2
通讯作者:
Mitchell GS
Mitchell GS
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Dale-Nagle EA;Hoffman MS;MacFarlane PM;Satriotomo I;Lovett-Barr MR;Vinit S;Mitchell GS

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可塑性是控制呼吸的神经系统的基本属性。呼吸可塑性的一个经常研究的模型是急性间歇性低氧(AIH)后的长期促进膈神经运动输出(PLTF)。PLTF产生于脊髓的可塑性,通过一种新的机制增加呼吸运动输出,这需要新的合成脑源性神经营养因子(BDNF),激活其高亲和力受体,原肌球蛋白相关蛋白B(TrkB)和细胞外相关蛋白(ERK)丝裂原激活蛋白(MAP)信号通路。由于间歇性低氧可诱导脊髓可塑性,我们正在探索利用重复性AIH作为一种手段,在导致呼吸功能不全的情况下诱导功能恢复,如颈椎损伤。由于反复AIH可诱导呼吸和运动神经元的表型可塑性,因此它可能恢复不完全脊髓损伤患者的呼吸运动功能。
Plasticity is a fundamental property of the neural system controlling breathing. One frequently studied model of respiratory plasticity is long-term facilitation of phrenic motor output (pLTF) following acute intermittent hypoxia (AIH). pLTF arises from spinal plasticity, increasing respiratory motor output through a mechanism that requires new synthesis of brain derived neurotrophic factor (BDNF), activation of its high affinity receptor, tropomyosin-related kinase B (TrkB) and extracellular-related kinase (ERK) mitogen-activated protein (MAP) kinase signaling in or near phrenic motor neurons. Since intermittent hypoxia induces spinal plasticity, we are exploring the potential to harness repetitive AIH as a means of inducing functional recovery in conditions causing respiratory insufficiency, such as cervical spinal injury. Since repetitive AIH induces phenotypic plasticity in respiratory and motor neurons, it may restore respiratory motor function in patients with incomplete spinal injury.
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