Sims Neil R, Yew Wai Ping
Centre for Neuroscience and Discipline of Medical Biochemistry, School of Medicine, Faculty of Medicine, Nursing and Health Sciences, Flinders University, Adelaide, South Australia, Australia.
Centre for Neuroscience and Discipline of Medical Biochemistry, School of Medicine, Faculty of Medicine, Nursing and Health Sciences, Flinders University, Adelaide, South Australia, Australia.
Neurochem Int. 2017 Jul;107:88-103. doi: 10.1016/j.neuint.2016.12.016. Epub 2017 Jan 3.
Alterations in neuronal connectivity, particularly in the "peri-infarct" tissue adjacent to the region of ischemic damage, are important contributors to the spontaneous recovery of function that commonly follows stroke. Peri-infarct astrocytes undergo reactive astrogliosis and play key roles in modulating the adaptive responses in neurons. This reactive astrogliosis shares many features with that induced by other forms of damage to the central nervous system but also differs in details that potentially influence neurological recovery. A subpopulation of astrocytes within a few hundred micrometers of the infarct proliferate and are centrally involved in the development of the glial scar that separates the damaged tissue in the infarct from surrounding normal brain. The intertwined processes of astrocytes adjacent to the infarct provide the core structural component of the mature scar. Interventions that cause early disruption of glial scar formation typically impede restoration of neurological function. Marked reactive astrogliosis also develops in cells more distant from the infarct but these cells largely remain in the spatial territories they occupied prior to stroke. These cells play important roles in controlling the extracellular environment and release proteins and other molecules that are able to promote neuronal plasticity and improve functional recovery. Treatments manipulating aspects of reactive astrogliosis can enhance neuronal plasticity following stroke. Optimising these treatments for use in human stroke would benefit from a more complete characterization of the specific responses of peri-infarct astrocytes to stroke as well as a better understanding of the influence of other factors including age, sex, comorbidities and reperfusion of the ischemic tissue.
神经元连接的改变，特别是在缺血性损伤区域附近的“梗死周围”组织中的改变，是中风后常见的功能自发恢复的重要促成因素。梗死周围的星形胶质细胞会发生反应性星形胶质增生，并在调节神经元的适应性反应中起关键作用。这种反应性星形胶质增生与中枢神经系统其他形式损伤所诱导的反应性星形胶质增生有许多共同特征，但在可能影响神经恢复的细节方面也有所不同。梗死灶几百微米范围内的一部分星形胶质细胞会增殖，并在将梗死灶中的受损组织与周围正常脑组织分隔开的胶质瘢痕形成过程中起核心作用。梗死灶附近星形胶质细胞相互交织的突起构成了成熟瘢痕的核心结构成分。导致胶质瘢痕形成早期破坏的干预措施通常会阻碍神经功能的恢复。在距离梗死灶较远的细胞中也会出现明显的反应性星形胶质增生，但这些细胞在很大程度上仍停留在中风前占据的空间区域。这些细胞在控制细胞外环境以及释放能够促进神经元可塑性和改善功能恢复的蛋白质和其他分子方面发挥重要作用。操纵反应性星形胶质增生相关方面的治疗可以增强中风后的神经元可塑性。若要优化这些治疗方法以用于人类中风，需要更全面地了解梗死周围星形胶质细胞对中风的具体反应，以及更好地理解包括年龄、性别、合并症和缺血组织再灌注等其他因素的影响。
