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首页> 外文期刊>Neuron >Peripheral demyelination and neuropathic pain behavior in periaxin-deficient mice.
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Peripheral demyelination and neuropathic pain behavior in periaxin-deficient mice.

机译:Periaxin缺陷小鼠的周围脱髓鞘和神经性疼痛行为。

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摘要

The Prx gene in Schwann cells encodes L- and S-periaxin, two abundant PDZ domain proteins thought to have a role in the stabilization of myelin in the peripheral nervous system (PNS). Mice lacking a functional Prx gene assemble compact PNS myelin. However, the sheath is unstable, leading to demyelination and reflex behaviors that are associated with the painful conditions caused by peripheral nerve damage. Older Prx-/- animals display extensive peripheral demyelination and a severe clinical phenotype with mechanical allodynia and thermal hyperalgesia, which can be reversed by intrathecal administration of a selective NMDA receptor antagonist We conclude that the periaxins play an essential role in stabilizing the Schwann cell-axon unit and that the periaxin-deficient mouse will be an important model for studying neuropathic pain in late onset demyelinating disease.
机译:Schwann细胞中的Prx基因编码L-和S-periaxin,这是两种丰富的PDZ域蛋白,被认为对稳定周围神经系统(PNS)中的髓磷脂具有作用。缺乏功能性Prx基因的小鼠组装紧凑的PNS髓磷脂。但是,护套不稳定,导致脱髓鞘和反射行为,与周围神经损伤引起的疼痛状况有关。较老的Prx-/-动物表现出广泛的外周脱髓鞘和严重的临床表型,并伴有机械性异常性疼痛和热痛觉过敏,可以通过鞘内注射选择性NMDA受体拮抗剂来逆转。轴突单位和periaxin缺陷小鼠将是研究迟发性脱髓鞘疾病的神经性疼痛的重要模型。

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