Epidural cerebellar stimulation drives widespread neural synchrony in the intact and stroke perilesional cortex.

Epidural cerebellar stimulation drives widespread neural synchrony in the intact and stroke perilesional cortex.
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DOI:
10.1186/s12984-021-00881-9
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发表时间:
2021-05-26
影响因子:
5.1
通讯作者:
Gulati T
Gulati T
中科院分区:
工程技术2区
文献类型:
--
作者:
Abbasi A;Danielsen NP;Leung J;Muhammad AKMG;Patel S;Gulati T

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在啮齿动物和人类研究中,小脑电刺激显示出改善中风后运动恢复的前景。过去的研究使用运动诱发电位(MEP)来评估小脑刺激如何调节皮层的持续活动,但其潜在机制尚未完全了解。在这里,我们使用侵入性电生理记录从完整的和中风受伤的啮齿动物初级运动皮层(M1),以评估如何硬膜外小脑刺激调制神经动力学在单神经元的水平,以及在中尺度动力学的水平。我们记录了单一的单位尖峰电位和局部场电位(LFPs)在完整的和急性中风损伤的M1对侧的成年Long-Evans大鼠在麻醉下的刺激小脑。我们分析了单个单位的放电率的变化,同步尖峰的程度和功率谱密度(PSD)的变化在LFPs期间和刺激后。我们的研究结果表明,刺激后,大多数M1神经元的放电率相对于其基线率发生了显着变化。这些放电率的变化是不同的性质,因为一些神经元的放电率增加,而其他减少。此外,这些变化在刺激期间开始出现。此外,交叉相关分析显示,神经元对之间的一致放电显着增加。有趣的是,这种同步性的增加与放电率变化的方向无关。我们还发现,通过主成分分析得到的神经元合奏更活跃的刺激后。最后,发生这些变化时,刺激后LFP的总体光谱功率没有显著变化。我们的结果表明,小脑刺激通过改变放电率、增强神经同步性和增加神经元组装的激活强度,导致M1神经元活动模式发生显着、持久的变化。我们的研究提供了证据,小脑刺激可以直接调节皮质动力学。由于这些结果存在于病灶周围皮层,我们的数据也可能有助于解释中风后小脑刺激的易化作用。
Cerebellar electrical stimulation has shown promise in improving motor recovery post-stroke in both rodent and human studies. Past studies have used motor evoked potentials (MEPs) to evaluate how cerebellar stimulation modulates ongoing activity in the cortex, but the underlying mechanisms are incompletely understood. Here we used invasive electrophysiological recordings from the intact and stroke-injured rodent primary motor cortex (M1) to assess how epidural cerebellar stimulation modulates neural dynamics at the level of single neurons as well as at the level of mesoscale dynamics. We recorded single unit spiking and local field potentials (LFPs) in both the intact and acutely stroke-injured M1 contralateral to the stimulated cerebellum in adult Long-Evans rats under anesthesia. We analyzed changes in the firing rates of single units, the extent of synchronous spiking and power spectral density (PSD) changes in LFPs during and post-stimulation. Our results show that post-stimulation, the firing rates of a majority of M1 neurons changed significantly with respect to their baseline rates. These firing rate changes were diverse in character, as the firing rate of some neurons increased while others decreased. Additionally, these changes started to set in during stimulation. Furthermore, cross-correlation analysis showed a significant increase in coincident firing amongst neuronal pairs. Interestingly, this increase in synchrony was unrelated to the direction of firing rate change. We also found that neuronal ensembles derived through principal component analysis were more active post-stimulation. Lastly, these changes occurred without a significant change in the overall spectral power of LFPs post-stimulation. Our results show that cerebellar stimulation caused significant, long-lasting changes in the activity patterns of M1 neurons by altering firing rates, boosting neural synchrony and increasing neuronal assemblies’ activation strength. Our study provides evidence that cerebellar stimulation can directly modulate cortical dynamics. Since these results are present in the perilesional cortex, our data might also help explain the facilitatory effects of cerebellar stimulation post-stroke.
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