Anatomical and neurophysiological evidence indicates that thoracic interneurons can serve a commissural function and activate contralateral motoneurons. Accordingly, we hypothesized that respiratory-related intercostal (IC) muscle electromyogram (EMG) activity would be only modestly impaired by a unilateral cervical spinal cord injury. Inspiratory tidal volume (VT) was recorded using pneumotachography and EMG activity was recorded bilaterally from the 1st to 2nd intercostal space in anesthetized, spontaneously breathing rats. Studies were conducted at 1–3 days, 2 wks or 8 wks following C2 spinal cord hemisection (C2HS). Data were collected during baseline breathing and a brief respiratory challenge (7% CO2). A substantial reduction in inspiratory intercostal EMG bursting ipsilateral to the lesion was observed at 1–3 days post-C2HS. However, a time-dependent return of activity occurred such that by 2 wks post-injury inspiratory intercostal EMG bursts ipsilateral to the lesion were similar to age-matched, uninjured controls. The increases in ipsilateral intercostal EMG activity occurred in parallel with increases in VT following the injury (R = 0.55; P < 0.001). We conclude that plasticity occurring within a “crossed-intercostal” circuitry enables a robust, spontaneous recovery of ipsilateral intercostal activity following C2HS in rats.
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机译：解剖学和神经生理学证据表明，胸部界面可以服务于偶然功能和激活对侧运动神经元。因此，我们假设呼吸相关的肋系统（IC）肌肉电肌（EMG）活性仅受到单侧宫颈脊髓损伤的谦虚损害。使用肺泡记录记录吸气的潮气量（VT），并在麻醉的，自发呼吸大鼠中从第一至第2肋肋间空间两侧记录EMG活性。在C2脊髓半联（C2HS）之后，在1-3天，2个WKS或8个WKS进行研究。在基线呼吸期间收集数据和短暂的呼吸攻击（7％CO2）。在C2HS后1-3天观察到在C 2 H后1-3天观察到吸气肋间EMG爆发滞后血管外侧的显着减少。然而，发生了时间依赖的活性回报，使得损伤后2个WKS损伤后肋系统的EMG爆发性损伤与病变类似于年龄匹配的未受约束对照。同侧肋间EMG活性的增加与损伤后vt的增加平行（r = 0.55; p <0.001）。我们得出结论，在“交叉肋间”电路内发生的可塑性使得在大鼠中C2HS之后的同侧肋间活性的稳健性，自发恢复。
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