时间：11月27日 (周四)  18:00-20:00

地点：恕园28号楼205室

主题：工作进展和文献报告

1、工作进展报告：外周衍生的TNF-α在调控小胶质细胞缺失小鼠神经病理性疼痛中的补偿作用

主讲：王姝燏 同学

2、工作进展报告：出生后发育早期少突胶质细胞前体细胞Neuroligin3在社交行为中的作用及其机制

主讲：葛嘉丽 同学

3、文献汇报：自由活动猕猴社会学习过程中视皮层与额叶皮层的互动

主讲：范宇 同学

4、文献汇报：小胶质细胞替换阻止小鼠和人类小胶质细胞源性疾病的发展

主讲：张译文 同学

欢迎老师与同学们踊跃出席！

脑科学研究所

文献详细信息

1、Visuo-frontal interactions during social learning in freely moving macaques

期刊信息：Nature   IF: 48.5   SCI: Q1   中科院：一区

摘要：

Social interactions represent a ubiquitous aspect of our everyday life that we acquire by interpreting and responding to visual cues from conspecifics. However, despite the general acceptance of this view, how visual information is used to guide the decision to cooperate is unknown. Here, we wirelessly recorded the spiking activity of populations of neurons in the visual and prefrontal cortex in conjunction with wireless recordings of oculomotor events while freely moving macaques engaged in social cooperation. As animals learned to cooperate, visual and executive areas refined the representation of social variables, such as the conspecific or reward, by distributing socially relevant information among neurons in each area. Decoding population activity showed that viewing social cues influences the decision to cooperate. Learning social events increased coordinated spiking between visual and prefrontal cortical neurons, which was associated with improved accuracy of neural populations to encode social cues and the decision to cooperate. These results indicate that the visual-frontal cortical network prioritizes relevant sensory information to facilitate learning social interactions while freely moving macaques interact in a naturalistic environment.

2、Microglia replacement halts the progression ofmicrogliopathy in mice and humans

期刊信息：Science IF：45.8   SCI：Q1 中科院：一区

摘要：

Colony-¬stimulating factor 1 receptor (CSF1R) is primarily expressed in microglia. Its monoallelic mutation causes CSF1R-¬associated microgliopathy (CAMP), a major form of adult-¬onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) and a fatal neurological disease without clinical cure. We developed mouse models harboring human hotspot mutations of CAMP and replaced CSF1R-¬deficient microglia through microglia replacement by bone marrow transplantation (Mr BMT), which attenuated pathology in mice. We further demonstrated that, in the context of CSF1R deficiency, traditional bone marrow transplantation (tBMT) in ALSP functions similarly to Mr BMT, efficiently replacing microglia and reducing disease progression. We then replaced CSF1R--deficient microglia in eight patients by tBMT. The disease progression was halted during the 4-¬month follow-¬up. Together, microglia replacement corrects pathogenic mutations and halts disease progression in mice and humans.