Department of Bioengineering, University of Pittsburgh, USA; Center for the Neural Basis of Cognition, Pittsburgh, PA, USA.
Veterans Administration Pittsburgh, Pittsburgh, PA, USA; Department of Neurology, University of Pittsburgh, USA.
Biomaterials. 2018 Nov;183:200-217. doi: 10.1016/j.biomaterials.2018.08.046. Epub 2018 Aug 22.
Oligodendrocytes and their precursors are critical glial facilitators of neurophysiology, which is responsible for cognition and behavior. Devices that are used to interface with the brain allow for a more in-depth analysis of how neurons and these glia synergistically modulate brain activity. As projected by the BRAIN Initiative, technologies that acquire a high resolution and robust sampling of neural signals can provide a greater insight in both the healthy and diseased brain and support novel discoveries previously unobtainable with the current state of the art. However, a complex series of inflammatory events triggered during device insertion impede the potential applications of implanted biosensors. Characterizing the biological mechanisms responsible for the degradation of intracortical device performance will guide novel biomaterial and tissue regenerative approaches to rehabilitate the brain following injury. Glial subtypes which assist with neuronal survival and exchange of electrical signals, mainly oligodendrocytes, their precursors, and the insulating myelin membranes they produce, are sensitive to inflammation commonly induced from insults to the brain. This review explores essential physiological roles facilitated by oligodendroglia and their precursors and provides insight into their pathology following neurodegenerative injury and disease. From this knowledge, inferences can be made about the impact of device implantation on these supportive glia in order to engineer effective strategies that can attenuate their responses, enhance the efficacy of neural interfacing technology, and provide a greater understanding of the challenges that impede wound healing and tissue regeneration during pathology.
少突胶质细胞及其前体细胞是神经生理学的关键神经胶质促进剂,对认知和行为负责。用于与大脑接口的设备可以更深入地分析神经元和这些神经胶质如何协同调节大脑活动。正如大脑倡议所预测的那样,能够获取高分辨率和强大的神经信号采样的技术可以为健康和患病的大脑提供更多的洞察力,并支持以前用现有技术无法获得的新发现。然而,在设备插入过程中引发的一系列复杂炎症事件阻碍了植入式生物传感器的潜在应用。对导致皮质内设备性能退化的生物学机制进行特征描述,将指导新型生物材料和组织再生方法,在受伤后恢复大脑功能。少突胶质细胞及其前体细胞和它们产生的绝缘髓鞘膜,协助神经元存活和电信号交换,对大脑损伤引起的炎症很敏感。这篇综述探讨了少突胶质细胞及其前体细胞所促进的基本生理作用,并深入了解了它们在神经退行性损伤和疾病后的病理学。从这些知识中,可以推断出设备植入对这些支持性神经胶质的影响,以便设计有效的策略来减轻它们的反应,增强神经接口技术的效果,并更好地理解在病理过程中阻碍伤口愈合和组织再生的挑战。