Phrenic motoneuron discharge patterns following chronic cervical spinal cord injury.

Phrenic motoneuron discharge patterns following chronic cervical spinal cord injury.
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DOI:
10.1016/j.expneurol.2013.08.003
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发表时间:
2013-11
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;Dougherty, Brendan J.;Sandhu, Milapjit S.;Lane, Michael A.;Reier, Paul J.;Fuller, David D.

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颈髓损伤(SCI)严重扰乱突触输入,触发与膈运动神经元(PhMN)池有关的生化、形态和可塑性。因此,我们的主要目的是确定慢性脊髓损伤是否会导致PHMN的招募情况和放电模式发生根本性变化。分别于损伤后2、4、8周记录麻醉成年雄性大鼠颈外侧(C2)半横断损伤(C2Hx)同侧膈神经的PhMN动作电位,并与对照组比较。根据放电模式,PhMN可分为早吸气(早吸气)或晚吸气(晚吸气)或静止型。在C2Hx之后,PhMN的分布以I型晚期细胞和静默细胞为主。迟发性猝发参数(例如,每次呼吸尖峰、猝发频率和持续时间)最初减少,但在损伤后8周恢复到控制值。此外,在C2Hx之后出现了一种独特的PhMN猝发模式,在低碳酸血症吸入性呼吸暂停期间,早期-I细胞强直地爆发。我们还量化了呼气末二氧化碳分压(PETCO2)逐渐降低对双侧膈神经活动的影响。与对照组相比,随着PETCO2的下降,C2Hx组动物的吸气频率(呼吸*分钟−1)更高,同侧膈肌爆发幅度更显著地下降。我们的结论是,C2Hx对同侧PhMN爆发模式的主要生理影响是持续的爆发延迟、爆发频率的一过性降低和紧张性爆发模式的出现。吸气频率数据表明,脑干网络的可塑性可能在颈椎脊髓损伤后的膈运动输出中发挥重要作用。
Cervical spinal cord injury (SCI) dramatically disrupts synaptic inputs and triggers biochemical, as well as morphological, plasticity in relation to the phrenic motor neuron (PhMN) pool. Accordingly, our primary purpose was to determine if chronic SCI induces fundamental changes in the recruitment profile and discharge patterns of PhMNs. Individual PhMN action potentials were recorded from the phrenic nerve ipsilateral to lateral cervical (C2) hemisection injury (C2Hx) in anesthetized adult male rats at 2, 4 or 8 wks post-injury and in uninjured controls. PhMNs were phenotypically classified as early (Early-I) or late inspiratory (Late-I), or silent according to discharge patterns. Following C2Hx, the distribution of PhMNs was dominated by Late-I and silent cells. Late-I burst parameters (e.g., spikes per breath, burst frequency and duration) were initially reduced but returned towards control values by 8 wks post-injury. In addition, a unique PhMN burst pattern emerged after C2Hx in which Early-I cells burst tonically during hypocapnic inspiratory apnea. We also quantified the impact of gradual reductions in end-tidal CO2 partial pressure (PETCO2) on bilateral phrenic nerve activity. Compared to control rats, as PETCO2 declined, the C2Hx animals had greater inspiratory frequencies (breaths*min−1) and more substantial decreases in ipsilateral phrenic burst amplitude. We conclude that the primary physiological impact of C2Hx on ipsilateral PhMN burst patterns is a persistent delay in burst onset, transient reductions in burst frequency, and the emergence of tonic burst patterns. The inspiratory frequency data suggest that plasticity in brainstem networks is likely to play an important role in phrenic motor output after cervical SCI.
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