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电刺激对非人类灵长类动物缺血性卒中的神经保护作用。

Neuroprotective Effects of Electrical Stimulation Following Ischemic Stroke in Non-Human Primates.

出版信息

Annu Int Conf IEEE Eng Med Biol Soc. 2022 Jul;2022:3085-3088. doi: 10.1109/EMBC48229.2022.9871335.

DOI:10.1109/EMBC48229.2022.9871335
PMID:36085944
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10259874/
Abstract

Brain stimulation has emerged as a novel therapy for ischemic stroke, a major cause of brain injury that often results in lifelong disability. Although past works in rodents have demonstrated protective effects of stimulation following stroke, few of these results have been replicated in humans due to the anatomical differences between rodent and human brains and a limited understanding of stimulation-induced network changes. Therefore, we combined electrophysiology and histology to study the neuroprotective mechanisms of electrical stimulation following cortical ischemic stroke in non-human primates. To produce controlled focal lesions, we used the photothrombotic method to induce targeted vasculature damage in the sensorimotor cortices of two macaques while collecting electrocorticography (ECoG) signals bilaterally. In another two monkeys, we followed the same lesioning procedures and applied repeated electrical stimulation via an ECoG electrode adjacent to the lesion. We studied the protective effects of stimulation on neural dynamics using ECoG signal power and coherence. In addition, we performed histological analysis to evaluate the differences in lesion volume. In comparison to controls, the ECoG signals showed decreased gamma power across the sensorimotor cortices in stimulated animals. Meanwhile, Nissl staining revealed smaller lesion volumes for the stimulated group, suggesting that electrical stimulation may exert neuroprotection by suppressing post-ischemic neural activity. With the similarity between NHP and human brains, this study paves the path for developing effective stimulation-based therapy for acute stroke in clinical studies.

摘要

脑刺激已成为缺血性中风的一种新疗法,缺血性中风是一种导致大脑损伤的主要原因,常常导致终身残疾。尽管过去在啮齿动物中的研究已经证明了刺激对中风后的保护作用,但由于啮齿动物和人类大脑之间的解剖差异以及对刺激诱导的网络变化的有限理解,这些结果很少在人类中得到复制。因此,我们结合电生理学和组织学研究了电刺激在非人灵长类动物皮质缺血性中风后的神经保护机制。为了产生受控的局灶性损伤,我们使用光血栓形成方法在两只猕猴的感觉运动皮质中诱导靶向血管损伤,同时收集双侧脑电皮层电图 (ECoG) 信号。在另外两只猴子中,我们遵循相同的损伤程序,并通过邻近损伤的 ECoG 电极施加重复的电刺激。我们使用 ECoG 信号功率和相干性研究刺激对神经动力学的保护作用。此外,我们进行了组织学分析以评估损伤体积的差异。与对照组相比,刺激动物的 ECoG 信号显示感觉运动皮质中的伽马功率降低。同时,尼氏染色显示刺激组的损伤体积较小,这表明电刺激可能通过抑制缺血后神经活动来发挥神经保护作用。由于 NHPs 和人类大脑之间的相似性,这项研究为在临床研究中开发有效的基于刺激的急性中风治疗方法铺平了道路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7dc/10259874/5d214113b6fe/nihms-1901334-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7dc/10259874/897f850f3f97/nihms-1901334-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7dc/10259874/f69dd4e83adc/nihms-1901334-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7dc/10259874/0ea9bd41a1e1/nihms-1901334-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7dc/10259874/5d214113b6fe/nihms-1901334-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7dc/10259874/897f850f3f97/nihms-1901334-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7dc/10259874/f69dd4e83adc/nihms-1901334-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7dc/10259874/0ea9bd41a1e1/nihms-1901334-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7dc/10259874/5d214113b6fe/nihms-1901334-f0004.jpg

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