时间：12月5日 (周五)  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：负性情绪的重复编码增强记忆的神经机制研究

主讲：朱晓曼 同学

2、工作进展报告：音乐旋律记忆及其脑机制研究工作进展汇报

主讲：余瑞 同学

3、文献汇报：小胶质细胞激活通过CXCL10介导的CD8+ T细胞募集促进衰老相关白质退化

主讲：陆洁莹 同学

4、文献汇报：小鼠的社交互动通过皮质-杏仁核神经环路延缓乳腺癌进展

主讲：许柯颍 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、题目：Microglia activation orchestrates CXCL10-mediated CD8+ T cell recruitment to promote aging-related white matter degeneration

期刊信息：Nature Neuroscience IF: 20.0 SCI: Q1 中科院：一区

摘要：

Aging is the major risk factor for neurodegeneration and is associated with structural and functional alterations in white matter. Myelin is particularly vulnerable to aging, resulting in white matter-associated microglia activation. Here we used pharmacological and genetic approaches to investigate microglial functions related to aging-associated changes in myelinated axons of mice. Our results reveal that maladaptive microglia activation promotes the accumulation of harmful CD8+ T cells, leading to the degeneration of myelinated axons and subsequent impairment of brain function and behavior. We characterize glial heterogeneity and aging-related changes in white matter by single-cell and spatial transcriptomics and reveal elaborate glial-immune interactions. Mechanistically, we show that the CXCL10-CXCR3 axis is crucial for the recruitment and retention of CD8+ T cells in aged white matter, where they exert pathogenic effects. Our results indicate that myelin-related microglia dysfunction promotes adaptive immune reactions in aging and identify putative targets to mitigate their detrimental impact.

2、题目：Social interaction in mice suppresses breast cancer progression via a corticoamygdala neural circuit

期刊信息：Neuron IF: 15.0 SCI: Q1 中科院：一区

摘要：

Social behaviors are vital for all mammalian species. Clinical observations and epidemiological studies have demonstrated that social interaction (SI) may slow cancer progression and improve patient outcomes. However, the underlying neural mechanisms remain unknown. Here, we found that SI in mouse models suppresses tumor growth through activating glutamatergic inputs from the anterior cingulate cortex (ACCGlu) to the basolateral amygdala (BLA), inhibiting intratumoral sympathetic nerve activity. Chemogenetic inhibition of the SI-activated ACCGlu neurons and ACCGlu→BLAGlu circuits abolished anxiolytic and antitumor effects of SI. Artificial reactivation of these neurons and circuits could mimic the anxiolytic and antitumor effects of SI. Manipulating the ACCGlu→BLAGlu circuits to regulate intratumoral sympathetic activity and norepinephrine (NE) release affected tumor progression by modulating antitumor immunity. Collectively, our study shows that SI activates the corticoamygdala neural circuit, which suppresses cancer progression, offering potential insights into the clinical application of social support in cancer treatment. （注：Glu为上标形式）