Hypoxia triggers short term potentiation of phrenic motoneuron discharge after chronic cervical spinal cord injury.

Hypoxia triggers short term potentiation of phrenic motoneuron discharge after chronic cervical spinal cord injury.
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缺氧会触发慢性宫颈脊髓损伤后的运动神经元排出的短期增强。

DOI:
10.1016/j.expneurol.2014.10.002
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发表时间:
2015-01
影响因子:
5.3
通讯作者:
Fuller, David D.
Fuller, David D.
中科院分区:
医学2区
文献类型:
--
作者:
Lee, Kun-Ze;Sandhu, Milapjit S.;Dougherty, Brendan J.;Reier, Paul J.;Fuller, David D.

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重复低氧暴露可诱导脊髓损伤后神经可塑性以及呼吸和躯体运动的恢复。本研究的目的是确定能力的一个单一的回合的缺氧引发短期可塑性的膈输出后,颈脊髓损伤,并确定膈运动神经元(PhrMN)的爆发和招聘模式的基础上的反应。在麻醉大鼠C2脊髓半切(C2 Hx)后11周,定量观察了低氧诱导的膈神经运动输出的短时程增强(STP)。3分钟低氧发作(12- 14%O2)总是触发吸气爆发振幅的STP,其幅度在C2 Hx同侧的膈爆发中大于对侧。我们接下来确定是否可以在C2 Hx同侧的募集(沉默)PhrMN中诱发STP。使用“单纤维”方法在缺氧期间和缺氧后记录单个PhrMN动作电位。爆发活动的STP没有发生在吸气开始时开始爆发的细胞中,但在招募的PhrMN以及在吸气努力后期开始爆发的先前活跃细胞中是稳健的。我们的结论是,在慢性C2 Hx之后,单次缺氧会触发同侧脊髓中PhrMNs的募集,并在缺氧暴露之后持续爆发。研究结果进一步支持了短期低氧作为SCI后神经康复训练方式的应用。
Repeated exposure to hypoxia can induce spinal neuroplasticity as well as respiratory and somatic motor recovery after spinal cord injury (SCI). The purpose of the present study was to define the capacity for a single bout of hypoxia to trigger short-term plasticity in phrenic output after cervical SCI, and to determine the phrenic motoneuron (PhrMN) bursting and recruitment patterns underlying the response. Hypoxia-induced short term potentiation (STP) of phrenic motor output was quantified in anesthetized rats 11 wks following lateral spinal hemisection at C2 (C2Hx). A 3-min hypoxic episode (12–14% O2) always triggered STP of inspiratory burst amplitude, the magnitude of which was greater in phrenic bursting ipsilateral vs. contralateral to C2Hx. We next determined if STP could be evoked in recruited (silent) PhrMNs ipsilateral to C2Hx. Individual PhrMN action potentials were recorded during and following hypoxia using a “single fiber” approach. STP of bursting activity did not occur in cells initiating bursting at inspiratory onset, but was robust in recruited PhrMNs as well as previously active cells initiating bursting later in the inspiratory effort. We conclude that following chronic C2Hx, a single bout of hypoxia triggers recruitment of PhrMNs in the ipsilateral spinal cord with bursting that persists beyond the hypoxic exposure. The results provide further support for the use of short bouts of hypoxia as a neurorehabilitative training modality following SCI.
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