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Mechanical Force Remodeling the Adult brain

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Neuroscience Bulletin 2023年第5期39卷 877-879页

作者： Chen Zhang Shuai Liu Yong-Chun Yu Qingjian Han state key laboratory of medical neurobiology and moe frontiers center for brain science Institutes of Brain ScienceFudan UniversityShanghai 200032China

The interactions between neural stem cells(NSCs)and their niche are essential for their maintenance,proliferation,differentiation,and migration,which contribute to brain plasticity,learning and memory,and cognition[1].As one of the key components of the NSC niche,astrocytes are vital in regulating the processes underlying brain development such as neuro-/gliogenesis,angiogenesis,axonal outgrowth,synaptogenesis,and synaptic pruning[2].Chemical and electrical signals mediated by adhesion molecules,the extracellular matrix,paracrine secretion.

关键词： vital maintenance migration

Signaling Mechanism for Modulation by GLP-1 and Exendin-4 of GABA Receptors on Rat Retinal Ganglion Cells

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Neuroscience Bulletin 2022年第6期38卷 622-636页

作者： Tao Zhang Hang-Ze Ruan Yong-Chen Wang Yu-Qi Shao Wei Zhou Shi-Jun Weng Yong-Mei Zhong state key laboratory of medical neurobiology and moe frontiers center for brain science Institutes of Brain ScienceFudan UniversityShanghai 200032.China

Glucagon-like peptide-1(GLP-1)is expressed in retinal neurons,but its role in the retina is largely unknown.Here,we demonstrated that GLP-1 or the GLP-1 receptor(GLP-1R;a G protein-coupled receptor)agonist exendin-4 suppressed-aminobutyric acid receptor(GABAR)-mediated currents through GLP-1Rs in isolated rat retinal ganglion cells(GCs).Pre-incubation with the stimulatory G protein(G,)inhibitor NF 449 abolished the exendin-4 effect.The exendin-4-induced suppression was mimicked by perfusion with 8-Br-cAMP(a cAMP analog),but was eliminated by the protein kinase A(PKA)inhibitor RpcAMP/KT-5720.The_exendin-4 effect was accompanied by an increase in[Ca2+];of GCs through the IP3-sensitive pathway and was blocked in Ca2+-free solution.Furthermore,when the activity of calmodulin(CaM)and CaMdependent protein kinase II(CaMKII)was inhibited,the exendin-4 effect was eliminated.Consistent with this,exendin-4 suppressed GABAR-mediated light-evoked inhibitory postsynaptic currents in GCs in rat retinal slices.These results suggest that exendin-4-induced suppression may be mediated by a distinct G,/cAMP-PKA/IPs/Ca+/CaM/CaMKIl signaling pathway,following the activation of GLP-1Rs.

关键词： Glucagon-like peptide-1 Exendin-4 GABA current Retinal ganglion cells Neuromodulation

TRPM7 Kinase Domain is Part of the Rac1-SSH2-cofilin Complex Regulating F-actin in the Mouse Nervous System

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Neuroscience Bulletin 2023年第6期39卷 989-993页

作者： Junzhuang Chang Cui Chen Wei Li Nashat Abumaria state key laboratory of medical neurobiology and moe frontiers center for brain science Department of Laboratory Animal ScienceInstitutes of Brain ScienceFudan UniversityShanghai200032China

Dear Editor,The ion channel transient receptor potential melastatin-like 7(TRPM7)has a serine-threonineα-kinase domain(M7CK)on its intracellular C-terminal[1,2].In cell lines,M7CK is cleaved and translocated to the nucleus to regulate a variety of cellular processes including cell proliferation and survival[3].In neuroblastoma cells.

关键词： Rac1 SSH2 neuroblastoma

Mechanosensitive Ion Channel TMEM63A Gangs Up with Local Macrophages to Modulate Chronic Post-amputation Pain

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Neuroscience Bulletin 2023年第2期39卷 177-193页

作者： Shaofeng Pu Yiyang Wu Fang Tong Wan-Jie Du Shuai Liu Huan Yang Chen Zhang Bin Zhou Ziyue Chen Xiaomeng Zhou Qingjian Han Dongping Du Pain Management center Shanghai Jiao Tong University Afliated Sixth People’s HospitalShanghai 200233China State Key Laboratory of Medical Neurobiology and MOE Frontier Center for Brain Science Institutes of Brain ScienceFudan UniversityShanghai 200032China

Post-amputation pain causes great sufering to amputees,but still no efective drugs are available due to its elusive mechanisms.Our previous clinical studies found that surgical removal or radiofrequency treatment of the neuroma at the axotomized nerve stump efectively relieves the phantom pain aficting patients after amputation.This indicated an essential role of the residual nerve stump in the formation of chronic post-amputation pain(CPAP).However,the molecular mechanism by which the residual nerve stump or neuroma is involved and regulates CPAP is still a mystery.In this study,we found that nociceptors expressed the mechanosensitive ion channel TMEM63A and macrophages infltrated into the dorsal root ganglion(DRG)neurons worked synergistically to promote CPAP.Histology and qRT-PCR showed that TMEM63A was mainly expressed in mechanical pain-producing non-peptidergic nociceptors in the DRG,and the expression of TMEM63A increased signifcantly both in the neuroma from amputated patients and the DRG in a mouse model of tibial nerve transfer(TNT).Behavioral tests showed that the mechanical,heat,and cold sensitivity were not afected in the Tmem63a-/-mice in the naïve state,suggesting the basal pain was not afected.In the infammatory and post-amputation state,the mechanical allodynia but not the heat hyperalgesia or cold allodynia was signifcantly decreased in Tmem63a-/-mice.Further study showed that there was severe neuronal injury and macrophage infltration in the DRG,tibial nerve,residual stump,and the neuromalike structure of the TNT mouse model,Consistent with this,expression of the pro-infammatory cytokines TNFα,IL-6,and IL-1βall increased dramatically in the DRG.Interestingly,the deletion of Tmem63a signifcantly reduced the macrophage infltration in the DRG but not in the tibial nerve stump.Furthermore,the ablation of macrophages signifcantly reduced both the expression of Tmem63a and the mechanical allodynia in the TNT mouse model,indicating an interaction between nociceptors and macrophages,and that these two

关键词： Mechanosensitive ion channel TMEM63A Post-amputation pain Tibial nerve transfer Macrophage

Enhancement of lysosome biogenesis as a potential therapeutic approach for neurodegenerative diseases

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Neural Regeneration Research 2023年第11期18卷 2370-2376页

作者： Wenlong Xue Jie Zhang Yang Li Department of Pharmacology State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain ScienceKey Laboratory of Metabolism and Molecular MedicineMinistry of EducationSchool of Basic Medical ScienceFudan UniversityShanghaiChina

Millions of people are suffering from Alzheimer’s disease globally,but there is still no effective treatment for this neurodegenerative disease.Thus,novel therapeutic approaches for Alzheimer’s disease are needed,which requires further evaluation of the regulato ry mechanisms of protein aggregate degradation.Lysosomes are crucial degradative organelles that maintain cellular homeostasis.Transcription factor EB-mediated lysosome biogenesis enhances autolysosomedependent degradation,which subsequently alleviates neurodege nerative diseases,including Alzheimer’s disease,Parkinson’s disease,and Huntington’s disease.In this review,we start by describing the key features of lysosomes,including their roles in nutrient sensing and degradation,and their functional impairments in different neurodegenerative diseases.We also explain the mechanisms—especially the post-translational modifications—which impact transcription factor EB and regulate lysosome biogenesis.Next,we discuss strategies for promoting the degradation of toxic protein aggregates.We describe Proteolysis-Ta rgeting Chimera and related technologies for the targeted degradation of specific proteins.We also introduce a group of LYsosome-Enhancing Compounds,which promote transcription factor EB-mediated lysosome biogenesis and improve learning,memory,and cognitive function in APP-PSEN1 mice.In summary,this review highlights the key aspects of lysosome biology,the mechanisms of transcription factor EB activation and lysosome biogenesis,and the promising strategies which are emerging to alleviate the pathogenesis of neurodegenerative diseases.

关键词： Alzheimer’s disease degradation lysosome biogenesis LYsosome-Enhancing Compounds neurodegenerative diseases post-translational modifications protein aggregates transcription factor EB

Roles of NG2 Glia in Cerebral Small Vessel Disease

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Neuroscience Bulletin 2023年第3期39卷 519-530页

作者： Yixi He Zhenghao Li Xiaoyu Shi Jing Ding Xin Wang Department of Neurology Zhongshan HospitalFudan UniversityShanghai 200032China state key laboratory of medical neurobiology and moe frontiers center for brain science Institutes of Brain ScienceFudan UniversityShanghai 200032China Institute of Neuroscience MOE Key Laboratory of Molecular NeurobiologyNMUShanghai 200433China

Cerebral small vessel disease(CSVD)is one of the most prevalent pathologic processes affecting 5%of people over 50 years of age and contributing to 45%of dementia cases.Increasing evidence has demonstrated the pathological roles of chronic hypoperfusion,impaired cerebral vascular reactivity,and leakage of the blood–brain barrier in CSVD.However,the pathogenesis of CSVD remains elusive thus far,and no radical treatment has been developed.NG2 glia,also known as oligodendrocyte precursor cells,are the fourth type of glial cell in addition to astrocytes,microglia,and oligodendrocytes in the mammalian central nervous system.Many novel functions for NG2 glia in physiological and pathological states have recently been revealed.In this review,we discuss the role of NG2 glia in CSVD and the underlying mechanisms.

关键词： NG2 glia Oligodendrocyte precursor cell Cerebral small vessel disease White matter injury

Developmental Origins of Human Cortical Oligodendrocytes and Astrocytes

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Neuroscience Bulletin 2022年第1期38卷 47-68页

作者： Lin Yang Zhenmeiyu Li Guoping Liu Xiaosu Li Zhengang Yang state key laboratory of medical neurobiology and moe frontiers center for brain science Institutes of Brain ScienceInstitute for Translational Brain Researchand Department of NeurologyZhongshan HospitalFudan UniversityShanghai200032China

Human cortical radial glial cells are primary neural stem cells that give rise to cortical glutaminergic projection pyramidal neurons, glial cells (oligodendrocytes and astrocytes) and olfactory bulb GABAergic interneurons. One of prominent features of the human cortex is enriched with glial cells, but there are major gaps in understanding how these glial cells are generated. Herein, by integrating analysis of published human cortical single-cell RNA-Seq datasets with our immunohistochemistical analyses, we show that around gestational week 18, EGFR-expressing human cortical truncated radial glial cells (tRGs) give rise to basal multipotent intermediate progenitors (bMIPCs) that express EGFR, ASCL1, OLIG2 and OLIG1. These bMIPCs undergo several rounds of mitosis and generate cortical oligodendrocytes, astrocytes and olfactory bulb interneurons. We also characterized molecular features of the cortical tRG. Integration of our findings suggests a general picture of the lineage progression of cortical radial glial cells, a fundamental process of the developing human cerebral cortex.

关键词： Radial glial cell Intermediate progenitor cell EGFR HOPX Oligodendrocyte Astrocyte Olfactory bulb interneuron Cerebral cortex Human

Cell-cycle length of medial ganglionic eminence progenitors contributes to interneuron fate

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Protein & Cell 2022年第2期13卷 141-147页

作者： Ni Zong Min Wang Yinghui Fu Dan Shen Yong-Chun Yu Jing’an District Central Hospital of Shanghai State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain ScienceInstitutes of Brain ScienceFudan UniversityShanghai 200032China

Dear Editor,GABAergic interneurons contribute to cortical function by regulating the balance of activity.Malfunction of inhibitory interneurons has been associated with neuropsychiatric disorders(Hashimoto et al.2003;Marín 2012).The most striking feature of GABAergic interneurons is their diversity of cell types.Although fate-mapping studies have demonstrated the presence of spatially and temporally distinct progenitor domains for interneuron subclasses within the embryonic ventral telencephalon(Butt et al.2005;Inan et al.2012),the mechanisms of interneuron subtype-determination during development remain poorly understood.

关键词： medial cycle striking

Lighting up Oxytocin Neurons to Nurture the brain

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Neuroscience Bulletin 2023年第5期39卷 866-868页

作者： Fang Zhou Junqiang Zheng Han Xu Department of neurobiology and Department of Neurology of the Second Affiliated Hospital Zhejiang University School of MedicineHangzhou 310058China Liangzhu laboratory MOE Frontier Science Center for Brain Science and Brain-machine IntegrationState Key Laboratory of Brain-machine IntelligenceZhejiang UniversityHangzhou 311121China NHC and CAMS key laboratory of medical neurobiology Zhejiang UniversityHangzhou 310058China

The sensory system develops earlier than the systems responsible for higher brain functions such as language and cognition[1].Moreover,sensory experiences in early life are critical for the development of the brain.However,how sensory experiences shape brain development is an important yet unresolved question in neuroscience.Previous work has demonstrated that deprivation of sensory inputs in the early developmental stage causes synaptic dysfunction in the sensory cortex.Interestingly,it has been reported that oxytocin can restore the deficits caused by somatosensory deprivation in neonatal mice,suggesting that oxytocin may play a key role in sensory-mediated synaptogenesis[2].Vision is one of the most important sensory inputs during early development in mammalians including humans[1],but the neural mechanism underlying vision-mediated brain development is still largely unknown.

关键词： neonatal neural sensory