胶质细胞调控视网膜损伤后的突触可塑性

多种类型的视网膜损伤除了引起神经元的改变外,还可诱导视网膜内突触发生可塑性变化。这些突触的形态或功能改变,可能是各种干预措施能保护神经元免于死亡,但却不能使受损的视觉功能有效恢复。中国中南大学周利红博士所在团队的一项研究显示,急性高眼压损伤模型中视网膜胶质细胞主动参与了急性高眼压损伤后视网膜内、外网层神经元突触的可塑性调控。

SICENCE新闻发布 作者：周利红 稿号：N201303025 胶质细胞调控视网膜损伤后的突触可塑性

多种类型的视网膜损伤除了引起神经元的改变外，还可诱导视网膜内突触发生可塑性变化。这些突触的形态或功能改变，可能是各种干预措施能保护神经元免于死亡，但却不能使受损的视觉功能有效恢复。中国中南大学周利红博士所在团队的一项研究显示，急性高眼压损伤模型中视网膜胶质细胞主动参与了急性高眼压损伤后视网膜内、外网层神经元突触的可塑性调控。胶质细胞在视网膜损伤后活化的现象一直以来都被认为与视网膜神经元死亡关系密切，可能与其活化后释放大量细胞有害物质有关。该项研究发现，在急性高眼压损伤后，视网膜内的胶质细胞明显活化，活化的胶质细胞可以明显上调视网膜内、外网层突触功能蛋白突触囊泡素的表达和分布。作者认为，在未来，胶质细胞有希望作为视网膜损伤后突触保护的一个新靶点。相关文章发表于2014年2月第4期发表《中国神经再生研究（英文版）》杂志。

而高眼压损伤3d后，大鼠视网膜内层明显变薄，突触囊泡素仍然分布于内网层的全层；且突触囊泡素在外网层的分布明显增宽增粗，且逐渐延伸到外核层的内侧部分

Article: " Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity," by Lihong Zhou, Hui Wang, Jia Luo, Kun Xiong, Leping Zeng, Dan Chen, Jufang Huang (Department of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, Hunan Province, China)

Zhou LH, Wang H, Luo J, Xiong K, Zeng LP, Chen D, Huang JF. Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity. Neural Regen Res. 2014;9(4):385-393.

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Regulatory effects of glial cells on retinal synaptic plasticity

Different types of retinal damage could induce plastic changes of retinal synapses, which might precede the serious damage of neuron soma. These morphological and functional changes to synapses after retinal injury could explain why many intervention measures protected neurons from death but failed to fully recover the damaged visual function. Therefore, it is necessary to investigate both the protection of synapses as well as protecting neurons from death. Dr. Lihong Zhou and co-workers from Central South University in China suggested that retinal glial cell activation might play an important role in the process of retinal synaptic plasticity induced by acute high intraocular pressure through affecting the expression and

多种类型的视网膜损伤除了引起神经元的改变外,还可诱导视网膜内突触发生可塑性变化。这些突触的形态或功能改变,可能是各种干预措施能保护神经元免于死亡,但却不能使受损的视觉功能有效恢复。中国中南大学周利红博士所在团队的一项研究显示,急性高眼压损伤模型中视网膜胶质细胞主动参与了急性高眼压损伤后视网膜内、外网层神经元突触的可塑性调控。

SICENCE新闻发布 作者：周利红 稿号：N201303025

distribution of synaptic functional proteins, such as synaptophysin. In their study, glial cells in the retina was activated in a rat model of acute ocular hypertension, and the expression of synaptophysin after high intraocular pressure induction showed a tendency of increase from the inner plexiform layer to the outer plexiform layer. Glial cells are promising as a new target to modulate retinal synaptic plasticity after retinal injury. The relevant paper has been published in the Neural Regeneration Research (Vol. 9, No. 4, 2014).

Synaptophysin immunoreactivity was still detectable across the entire inner plexiform layer and the inner plexiform layer had clearly thinned following 3 days of high intraocular pressure induction. In the outer plexiform layer, after 3 days of high intraocular pressure induction, synaptophysin immunoreactivity had spread and extended into the inner part of the outer nuclear layer.

Article: " Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity," by Lihong Zhou, Hui Wang, Jia Luo, Kun Xiong, Leping Zeng, Dan Chen, Jufang Huang (Department of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, Hunan Province, China)

Zhou LH, Wang H, Luo J, Xiong K, Zeng LP, Chen D, Huang JF. Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity. Neural Regen Res. 2014;9(4):385-393.