期刊,神经科学通报（英文版） 2023年卷2期_国家学术搜索

期刊信息/Journal information

神经科学通报（英文版）

主　　编：路长林(常务) 李朝义赵志奇

出版周期：双月刊

国际刊号：1673-7067

电子邮箱：nsb@sibs.ac.cn

电　　话：021-54922863

邮政编码：200031

地　　址：上海市岳阳路319号31B楼405室

神经科学通报（英文版）/Journal Neuroscience BulletinCSCDCSTPCD北大核心SCI

查看更多>>本刊被列入国家科技部“中国科技论文统计源期刊”，为“中国学术期刊（光盘版）收录期刊”和“万方数据——数字化期刊群”入网期刊。本刊以交流若干基础与临床神经科学实验研究成果，推动神经科学事业的发展为宗旨，以突出基础、兼顾临床、包容性强、读者面宽为特色。本刊编委会阵容强大，共有9名院士担纲，以确保期刊质量。

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

Shaofeng PuYiyang WuFang TongWan-Jie Du...

177-193页

查看更多>>摘要：Post-amputation pain causes great suffering to amputees,but still no effective 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 effectively relieves the phan-tom pain afflicting patients after amputation.This indicated an essential role of the residual nerve stump in the forma-tion 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 mecha-nosensitive ion channel TMEM63A and macrophages infil-trated into the dorsal root ganglion(DRG)neurons worked synergistically to promote CPAP.Histology and qRT-PCR showed that TMEM63A was mainly expressed in mechani-cal pain-producing non-peptidergic nociceptors in the DRG,and the expression of TMEM63A increased significantly 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 affected in the Tmem63a--/-mice in the naïve state,suggesting the basal pain was not affected.In the inflamma-tory and post-amputation state,the mechanical allodynia but not the heat hyperalgesia or cold allodynia was significantly decreased in Tmem63a-/-mice.Further study showed that there was severe neuronal injury and macrophage infiltration in the DRG,tibial nerve,residual stump,and the neuroma-like structure of the TNT mouse model,Consistent with this,expression of the pro-inflammatory cytokines TNF-α,IL-6,and IL-1 β all increased dramatically in the DRG.Interestingly,the deletion of Tmem63a significantly reduced the macrophage infiltration in the DRG but not in the tibial nerve stump.Furthermore,the ablation of macrophages significantly reduced both the expression of Tmem63a and the mechanical allodynia in the TNT mouse model,indicat-ing an interaction between nociceptors and macrophages,and that these two factors gang up together to regulate the formation of CPAP.This provides a new insight into the mechanisms underlying CPAP and potential drug targets its treatment.

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维普

miR-34b-3p Inhibition of eIF4E Causes Post-stroke Depression in Adult Mice

Xiao KeManfei DengZhuoze WuHongyan Yu...

194-212页

查看更多>>摘要：Post-stroke depression(PSD)is a serious and common complication of stroke,which seriously affects the rehabilitation of stroke patients.To date,the pathogenesis of PSD is unclear and effective treatments remain unavailable.Here,we established a mouse model of PSD through photothrombosis-induced focal ischemia.By using a combination of brain imaging,transcriptome sequencing,and bioinformatics analysis,we found that the hippocampus of PSD mice had a significantly lower metabolic level than other brain regions.RNA sequenc-ing revealed a significant reduction of miR34b-3p,which was expressed in hippocampal neurons and inhibited the translation of eukaryotic translation initiation factor 4E(eIF4E).Furthermore,silencing eIF4E inactivated microglia,inhibited neuroinflammation,and abolished the depression-like behaviors in PSD mice.Together,our data demonstrated that insufficient miR34b-3p after stroke cannot inhibit eIF4E translation,which causes PSD by the activation of microglia in the hippocampus.Therefore,miR34b-3p and eIF4E may serve as potential therapeutic targets for the treatment of PSD.

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Spatiotemporal Dynamics of the Molecular Expression Pattern and Intercellular Interactions in the Glial Scar Response to Spinal Cord Injury

Leilei GongYun GuXiaoxiao HanChengcheng Luan...

213-244页

查看更多>>摘要：Nerve regeneration in adult mammalian spinal cord is poor because of the lack of intrinsic regeneration of neurons and extrinsic factors-the glial scar is triggered by injury and inhibits or promotes regeneration.Recent tech-nological advances in spatial transcriptomics(ST)provide a unique opportunity to decipher most genes systematically throughout scar formation,which remains poorly under-stood.Here,we first constructed the tissue-wide gene expres-sion patterns of mouse spinal cords over the course of scar formation using ST after spinal cord injury from 32 sam-ples.Locally,we profiled gene expression gradients from the leading edge to the core of the scar areas to further under-stand the scar microenvironment,such as neurotransmitter disorders,activation of the pro-inflammatory response,neu-rotoxic saturated lipids,angiogenesis,obstructed axon exten-sion,and extracellular structure re-organization.In addi-tion,we described 21 cell transcriptional states during scar formation and delineated the origins,functional diversity,and possible trajectories of subpopulations of fibroblasts,glia,and immune cells.Specifically,we found some regu-lators in special cell types,such as Thbs1 and Colla2 in macrophages,CD36 and Postn in fibroblasts,Plxnb2 and Nxpe3 in microglia,Clu in astrocytes,and CD74 in oligo-dendrocytes.Furthermore,salvianolic acid B,a blood-brain barrier permeation and CD36 inhibitor,was administered after surgery and found to remedy fibrosis.Subsequently,we described the extent of the scar boundary and profiled the bidirectional ligand-receptor interactions at the neighboring cluster boundary,contributing to maintain scar architecture during gliosis and fibrosis,and found that GPR37L1_PSAP,and GPR37_PSAP were the most significant gene-pairs among microglia,fibroblasts,and astrocytes.Last,we quan-tified the fraction of scar-resident cells and proposed four possible phases of scar formation:macrophage infiltration,proliferation and differentiation of scar-resident cells,scar emergence,and scar stationary.Together,these profiles delineated the spatial heterogeneity of the scar,confirmed the previous concepts about scar architecture,provided some new clues for scar formation,and served as a valuable resource for the treatment of central nervous system injury.

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Somatostatin-Positive Neurons in the Rostral Zona Incerta Modulate Innate Fear-Induced Defensive Response in Mice

Shan LinMeng-Yue ZhuMeng-Yu TangMi Wang...

245-260页

查看更多>>摘要：Defensive behaviors induced by innate fear or Pavlovian fear conditioning are crucial for animals to avoid threats and ensure survival.The zona incerta(ZI)has been demonstrated to play important roles in fear learning and fear memory,as well as modulating auditory-induced innate defensive behavior.However,whether the neuronal subtypes in the ZI and specific circuits can mediate the innate fear response is largely unknown.Here,we found that somato-statin(SST)-positive neurons in the rostral ZI of mice were activated by a visual innate fear stimulus.Optogenetic inhi-bition of SST-positive neurons in the rostral ZI resulted in reduced flight responses to an overhead looming stimulus.Optogenetic activation of SST-positive neurons in the rostral ZI induced fear-like defensive behavior including increased immobility and bradycardia.In addition,we demonstrated that manipulation of the GABAergic projections from SST-positive neurons in the rostral ZI to the downstream nucleus reuniens(Re)mediated fear-like defensive behavior.Ret-rograde trans-synaptic tracing also revealed looming stim-ulus-activated neurons in the superior colliculus(SC)that projected to the Re-projecting SST-positive neurons in the rostral ZI(SC-ZIrSST-Re pathway).Together,our study elu-cidates the function of SST-positive neurons in the rostral ZI and the SC-ZIrSST-Re tri-synaptic circuit in mediating the innate fear response.

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Elevated Levels of Naturally-Occurring Autoantibodies Against the Extracellular Domain of p75NTR Aggravate the Pathology of Alzheimer's Disease

Chen-Yang HeDing-Yuan TianSi-Han ChenWang-Sheng Jin...

261-272页

查看更多>>摘要：The extracellular domain(p75ECD)of p75 neu-rotrophin receptor(p75NTR)antagonizes Aβ neurotoxicity and promotes Aβ clearance in Alzheimer's disease(AD).The impaired shedding of p75ECD is a key pathological process in AD,but its regulatory mechanism is largely unknown.This study was designed to investigate the pres-ence and alterations of naturally-occurring autoantibodies against p75ECD(p75ECD-NAbs)in AD patients and their effects on AD pathology.We found that the cerebrospinal fluid(CSF)level of p75ECD-NAbs was increased in AD,and negatively associated with the CSF levels of p75ECD.Transgenic AD mice actively immunized with p75ECD showed a lower level of p75ECD and more severe AD pathology in the brain,as well as worse cognitive functions than the control groups,which were immunized with Re-p75ECD(the reverse sequence of p75ECD)and phosphate-buffered saline,respectively.These findings demonstrate the impact of p75ECD-NAbs on p75NTR/p75ECD imbalance,providing a novel insight into the role of autoimmunity and p75NTR in AD.

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MAGED4B Promotes Glioma Progression via Inactivation of the TNF-α-induced Apoptotic Pathway by Down-regulating TRIM27 Expression

Can LiuJun LiuJuntang ShaoCheng Huang...

273-291页

查看更多>>摘要：MAGED4B belongs to the melanoma-associated antigen family;originally found in melanoma,it is expressed in various types of cancer,and is especially enriched in glioblastoma.However,the functional role and molecular mechanisms of MAGED4B in glioma are still unclear.In this study,we found that the MAGED4B level was higher in glioma tissue than that in non-cancer tissue,and the level was positively correlated with glioma grade,tumor diameter,Ki-67 level,and patient age.The patients with higher levels had a worse prognosis than those with lower MAGED4B levels.In glioma cells,MAGED4B overexpression promoted proliferation,invasion,and migration,as well as decreas-ing apoptosis and the chemosensitivity to cisplatin and temozolomide.On the contrary,MAGED4B knockdown in glioma cells inhibited proliferation,invasion,and migration,as well as increasing apoptosis and the chemosensitivity to cisplatin and temozolomide.MAGED4B knockdown also inhibited the growth of gliomas implanted into the rat brain.The interaction between MAGED4B and tripartite motif-containing 27(TRIM27)in glioma cells was detected by co-immunoprecipitation assay,which showed that MAGED4B was co-localized with TRIM27.In addition,MAGED4B overexpression down-regulated the TRIM27 protein level,and this was blocked by carbobenzoxyl-L-leucyl-L-leucyl-L-leucine(MG132),an inhibitor of the proteasome.On the contrary,MAGED4B knockdown up-regulated the TRIM27 level.Furthermore,MAGED4B overexpression increased TRIM27 ubiquitination in the presence of MG132.Accord-ingly,MAGED4B down-regulated the protein levels of genes downstream of ubiquitin-specific protease 7(USP7)involved in the tumor necrosis factor-alpha(TNF-α)-induced apoptotic pathway.These findings indicate that MAGED4B promotes glioma growth via a TRIM27/USP7/receptor-inter-acting serine/threonine-protein kinase 1(RIPl)-dependent TNF-α-induced apoptotic pathway,which suggests that MAGED4B is a potential target for glioma diagnosis and treatment.

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Connectivity Map of Subthalamic Corticotropin-releasing Hormone Neurons in the Mouse Brain

Yu-Ting TsengLisha LiangBinghao ZhaoJialin Ye...

292-296页

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Extension of the Lifespan of a Mouse Model of Rett Syndrome by Intracerebroventricular Delivery of MECP2

Kan YangCheng ChengYiting YuanYuefang Zhang...

297-302页

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Mechanisms Underlying Brain Aging Under Normal and Pathological Conditions

Menglong JinShi-Qing Cai

303-314页

查看更多>>摘要：Aging is a major risk factor for many human diseases,including cognitive impairment,which affects a large population of the elderly.In the past few decades,our understanding of the molecular and cellular mechanisms underlying the changes associated with aging and age-related diseases has expanded greatly,shedding light on the potential role of these changes in cognitive impairment.In this article,we review recent advances in understanding of the mechanisms underlying brain aging under normal and pathological conditions,compare their similarities and dif-ferences,discuss the causative and adaptive mechanisms of brain aging,and finally attempt to find some rules to guide us on how to promote healthy aging and prevent age-related diseases.

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Neural Correlates of Spatial Navigation in Primate Hippocampus

Dun Mao

315-327页

查看更多>>摘要：The hippocampus has been extensively impli-cated in spatial navigation in rodents and more recently in bats.Numerous studies have revealed that various kinds of spatial information are encoded across hippocampal regions.In contrast,investigations of spatial behavioral correlates in the primate hippocampus are scarce and have been mostly limited to head-restrained subjects during virtual navigation.However,recent advances made in freely-moving primates suggest marked differences in spatial representations from rodents,albeit some similarities.Here,we review empirical studies examining the neural correlates of spatial naviga-tion in the primate(including human)hippocampus at the levels of local field potentials and single units.The lower frequency theta oscillations are often intermittent.Single neuron responses are highly mixed and task-dependent.We also discuss neuronal selectivity in the eye and head coor-dinates.Finally,we propose that future studies should focus on investigating both intrinsic and extrinsic population activ-ity and examining spatial coding properties in large-scale hippocampal-neocortical networks across tasks.

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维普