Neural interface technology provides direct sampling and analysis of electrical and chemical events in the brain in order to better understand neuronal function and treat neurodegenerative disease. However, intracortical electrodes experience inflammatory reactions that reduce long-term stability and functionality and are understood to be facilitated by activated microglia and astrocytes. Emerging studies have identified another cell type that participates in the formation of a high-impedance glial scar following brain injury; the oligodendrocyte precursor cell (OPC). These cells maintain functional synapses with neurons and are a crucial source of neurotrophic support. Following injury, OPCs migrate toward areas of tissue injury over the course of days, similar to activated microglia. The delayed time course implicates these OPCs as key components in the formation of the outer layers of the glial scar around the implant. In vivo two-photon laser scanning microscopy (TPLSM) was employed to observe fluorescently-labeled OPC and microglia reactivity up to 72 h following probe insertion. OPCs initiated extension of cellular processes (2.5 ± 0.4 μm h⁻¹) and cell body migration (1.6 ± 0.3 μm h⁻¹) toward the probe beginning 12 h after insertion. By 72 h, OPCs became activated at a radius of about 190.3 μm away from the probe surface. This study characterized the early spatiotemporal dynamics of OPCs involved in the inflammatory response induced by microelectrode insertion. OPCs are key mediators of tissue health and are understood to have multiple fate potentials. Detailed spatiotemporal characterization of glial behavior under pathological conditions may allow identification of alternative intervention targets for mitigating the formation of a glial scar and subsequent neurodegeneration that debilitates chronic neural interfaces.

神经接口技术可对大脑中的电和化学事件进行直接采样和分析，以便更好地了解神经元功能并治疗神经退行性疾病。然而，皮质内电极会经历炎症反应，从而降低长期稳定性和功能性，并且被认为是由激活的小胶质细胞和星形胶质细胞促进的。新兴研究发现另一种细胞类型参与脑损伤后高阻抗神经胶质疤痕的形成；少突胶质细胞前体细胞（OPC）。这些细胞与神经元维持功能性突触，是神经营养支持的重要来源。损伤后，OPC 在几天内会向组织损伤区域迁移，类似于激活的小胶质细胞。延迟的时间过程表明这些OPC是植入物周围神经胶质疤痕外层形成的关键成分。采用体内双光子激光扫描显微镜 (TPLSM) 观察探针插入后 72 小时内荧光标记的 OPC 和小胶质细胞的反应性。插入后 12 小时开始，OPC 开始向探针延伸细胞过程 (2.5 ± 0.4 μm h ^-1 ) 和细胞体迁移 (1.6 ± 0.3 μm h ^-1 )。 72 小时后，OPC 在距离探针表面约 190.3 μm 的半径处被激活。本研究描述了参与微电极插入诱导的炎症反应的 OPC 的早期时空动态。 OPC 是组织健康的关键介质，并且被认为具有多种命运潜力。 病理条件下神经胶质行为的详细时空特征可能有助于识别替代干预目标，以减轻神经胶质疤痕的形成和随后使慢性神经界面衰弱的神经变性。