Zelenin Pavel V, Lyalka Vladimir F, Orlovsky Grigori N, Deliagina Tatiana G
Department of Neuroscience, Karolinska Institute, Stockholm, Sweden.
Front Cell Neurosci. 2019 Aug 21;13:387. doi: 10.3389/fncel.2019.00387. eCollection 2019.
Postural limb reflexes (PLRs) are an essential component of postural corrections. Spinalization leads to disappearance of postural functions (including PLRs). After spinalization, spastic, incorrectly phased motor responses to postural perturbations containing oscillatory EMG bursting gradually develop, suggesting plastic changes in the spinal postural networks. Here, to reveal these plastic changes, rabbits at 3, 7, and 30 days after spinalization at T12 were decerebrated, and responses of spinal interneurons from L5 along with hindlimb muscles EMG responses to postural sensory stimuli, causing PLRs in subjects with intact spinal cord (control), were characterized. Like in control and after acute spinalization, at each of three studied time points after spinalization, neurons responding to postural sensory stimuli were found. Proportion of such neurons during 1st month after spinalization did not reach the control level, and was similar to that observed after acute spinalization. In contrast, their activity (which was significantly decreased after acute spinalization) reached the control value at 3 days after spinalization and remained close to this level during the following month. However, the processing of postural sensory signals, which was severely distorted after acute spinalization, did not recover by 30 days after injury. In addition, we found a significant enhancement of the oscillatory activity in a proportion of the examined neurons, which could contribute to generation of oscillatory EMG bursting. Motor responses to postural stimuli (which were almost absent after acute spinalization) re-appeared at 3 days after spinalization, although they were very weak, irregular, and a half of them was incorrectly phased in relation to postural stimuli. Proportion of correct and incorrect motor responses remained almost the same during the following month, but their amplitude gradually increased. Thus, spinalization triggers two processes of plastic changes in the spinal postural networks: rapid (taking days) restoration of normal activity level in spinal interneurons, and slow (taking months) recovery of motoneuronal excitability. Most likely, recovery of interneuronal activity underlies re-appearance of motor responses to postural stimuli. However, absence of recovery of normal processing of postural sensory signals and enhancement of oscillatory activity of neurons result in abnormal PLRs and loss of postural functions.
肢体姿势反射(PLRs)是姿势矫正的重要组成部分。脊髓横断会导致姿势功能(包括PLRs)消失。脊髓横断后,对包含振荡性肌电图爆发的姿势扰动会逐渐出现痉挛性、相位错误的运动反应,这表明脊髓姿势网络发生了可塑性变化。在此,为了揭示这些可塑性变化,对T12脊髓横断后3天、7天和30天的兔子进行了去大脑处理,并对来自L5的脊髓中间神经元的反应以及后肢肌肉对姿势感觉刺激的肌电图反应进行了表征,这些刺激在脊髓完整的受试者(对照组)中会引发PLRs。与对照组和急性脊髓横断后一样,在脊髓横断后的三个研究时间点中的每一个时间点,都发现了对姿势感觉刺激有反应的神经元。脊髓横断后第一个月此类神经元的比例未达到对照组水平,且与急性脊髓横断后观察到的比例相似。相比之下,它们的活动(急性脊髓横断后显著降低)在脊髓横断后3天达到对照组值,并在接下来的一个月内保持接近该水平。然而,急性脊髓横断后严重扭曲的姿势感觉信号处理在损伤后30天并未恢复。此外,我们发现一部分被检查神经元的振荡活动显著增强,这可能有助于振荡性肌电图爆发的产生。对姿势刺激的运动反应(急性脊髓横断后几乎不存在)在脊髓横断后3天重新出现,尽管它们非常微弱、不规则,并且其中一半与姿势刺激的相位错误。在接下来的一个月内,正确和错误运动反应的比例几乎保持不变,但它们的幅度逐渐增加。因此,脊髓横断触发了脊髓姿势网络中两个可塑性变化过程:脊髓中间神经元正常活动水平的快速(数天)恢复,以及运动神经元兴奋性的缓慢(数月)恢复。最有可能的是,中间神经元活动的恢复是对姿势刺激的运动反应重新出现的基础。然而,姿势感觉信号正常处理未恢复以及神经元振荡活动增强导致了异常的PLRs和姿势功能丧失。