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PCDH17 restricts dendritic spine morphogenesis by regulating ROCK2-dependent control of the actin cytoskeleton,modulating emotional behavior

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Zoological Research 2024年第3期45卷 535-550页

作者： Laidong Yu Fangfang Zeng Mengshu Fan Kexuan Zhang Jingjing Duan Yalu Tan Panlin Liao Jin Wen Chenyu Wang Meilin Wang Jialong Yuan Xinxin Pang Yan Huang Yangzhou Zhang Jia-Da Li Zhuohua Zhang Zhonghua Hu Hunan Key Laboratory of Molecular Precision Medicine Department of Critical Care MedicineXiangya HospitalCentral South UniversityChangshaHunan 410008China Center for Medical Genetics and Hunan Key Laboratory of Medical Genetics School of Life SciencesCentral South UniversityChangshaHunan 410008China National Clinical Research Center for Geriatric Disorders Xiangya HospitalCentral South UniversityChangshaHunan 410008China Hunan Provincial Clinical Research Center for Critical Care Medicine Xiangya HospitalCentral South UniversityChangshaHunan 410008China Hunan Key Laboratory of Animal Models for Human Diseases School of Life SciencesCentral South UniversityChangshaHunan 410008China MOE Key Lab of Rare Pediatric Diseases School of Life SciencesCentral South UniversityChangshaHunan 410008China Department of Neurosciences University of South China Medical SchoolHengyangHunan 421001China

Proper regulation of synapse formation and elimination is critical for establishing mature neuronal circuits and maintaining brain *** abnormalities,such as defects in the density and morphology of postsynaptic dendritic spines,underlie the pathology of various neuropsychiatric *** 17(PCDH17)is associated with major mood disorders,including bipolar disorder and ***,the molecular mechanisms by which PCDH17 regulates spine number,morphology,and behavior remain *** this study,we found that PCDH17 functions at postsynaptic sites,restricting the number and size of dendritic spines in excitatory *** overexpression of PCDH17 in the ventral hippocampal CA1 results in spine loss and anxiety-and depression-like behaviors in ***,PCDH17 interacts with actin-relevant proteins and regulates actin filament(F-actin)***,PCDH17 binds to ROCK2,increasing its expression and subsequently enhancing the activity of downstream targets such as LIMK1 and the phosphorylation of cofilin serine-3(Ser3).Inhibition of ROCK2 activity with belumosudil(KD025)ameliorates the defective F-actin organization and spine structure induced by PCDH17 overexpression,suggesting that ROCK2 mediates the effects of PCDH17 on F-actin content and spine ***,these findings reveal a novel mechanism by which PCDH17 regulates synapse development and behavior,providing pathological insights into the neurobiological basis of mood disorders.

关键词： Synapse development dendritic spine Mood disorder Actin cytoskeleton Animal behavior

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Epigenetic regulation of neuronal dendrite and dendritic spine development

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Frontiers in Biology 2010年第4期5卷 304-323页

作者： Richard D.SMRT Xinyu ZHAO Department of Neuroscience University of New Mexico School of MedicineAlbuquerqueNew Mexico 87131USA

Dendrites and the dendritic spines of neurons play key roles in the connectivity of the brain and have been recognized as the locus of long-term synaptic plasticity,which is correlated with learning and *** development of dendrites and spines in the mammalian central nervous system is a complex process that requires specific molecular events over a period of *** has been shown that specific molecules are needed not only at the spine’s point of contact,but also at a distance,providing signals that initiate a cascade of events leading to synapse *** specific molecules that act to signal neuronal differentiation,dendritic morphology,and synaptogenesis are tightly regulated by genetic and epigenetic *** has been shown that the dendritic spine structure and distribution are altered in many diseases,including many forms of mental retardation(MR),and can also be potentiated by neuronal activities and an enriched *** dendritic spine pathologies are found in many types of MR,it has been proposed that an inability to form normal spines leads to the cognitive and motor deficits that are characteristic of *** mechanisms,including DNA methylation,chromatin remodeling,and the noncoding RNA-mediated process,have profound regulatory roles in mammalian gene *** study of epigenetics focuses on cellular effects that result in a heritable pattern of gene expression without changes to genomic *** extensive efforts to understand the molecular regulation of dendrite and spine development,epigenetic mechanisms have only recently been *** this review,we will focus on epigenetic mechanisms that regulate the development and maturation of dendrites and *** will discuss how epigenetic alterations could result in spine abnormalities that lead to MR,such as is seen in fragile X and Rett *** will also discuss both general methodology and recent technological advances in the study of neuronal den

关键词： epigenetics neurodevelopment dendritic spine synapse microRNA methyl-CpG binding protein 2(MeCP2) mental retardation

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dendritic spine pathology in autism： lessons learned from mouse models

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Journal of Translational Neuroscience 2016年第2期1卷 21-37页

作者： Qiangge Zhang Dingxi Zhou Guoping Feng McGovern Institutefor Brain Research Department of Brainand Cognitive SciencesMassachusetts Institute of TechnologyCambridgeMA02139USA Stanley Center for Psychiatric Research Broad Institute of MIT and HarvardCambridgeMA02142USA School of Life Sciences Peking UniversityBeijing 100871China

Autism spectrum disorders （ASD） are a group of neurodevelopmental disorders that affect up to 1.5% of population in the world. Recent large scale genomic studies show that genetic causes of ASD are very heterogeneous. Gene ontology, pathway analysis and animal model studies have revealed several potential converging mechanisms including postsynaptic dysfunction of excitatory synapses. In this review, we focus on the structural and functional specializations of dendritic spines, and describe their defects in ASD. We use Fragile X syndrome, Rett syndrome and Phe- lan-McDermid syndrome, three of the most studied neurodevelopmental disorders with autism features, as examples to demonstrate the significant contribution made by mouse models towards the understanding of monogenic ASD. We envision that the development and application of new technologies to study the function ofdendritic spines in valid animal models wi l l eventually lead to innovative treatments for ASD.

关键词： synapse dendritic spine autism FMRlt MECP2t SHANKS animal model

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Opposing dendritic spine plasticity of fear learning and unlearning in neocortex

Opposing dendritic spine plasticity of fear learning and unl...

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中国生理学会第24届全国会员代表大会暨生理学学术大会

作者： Cora Sau Wan Lai Department of Physiology LKS Faculty of MedicineThe University of Hong Kong

Fear conditioning is an associative learning in which a conditioned neutral stimulus is paired with an aversive unconditioned stimulus to elicit fear *** exposures to conditioned stimulus diminish the expression of fear response,a process called *** it is generally believed that fear extinction is a form of new learning that inhibits rather than erases previously acquired fear memories,the hypothesis that extinction causes the partial erasure of fear memories remains *** investigate how neural circuits are modified by fear learning and extinction,we used transcranial two-photon microscopy to examine the formation and elimination of postsynaptic dendritic spines of layer V pyramidal neurons in mouse *** found that fear conditioning by pairing an auditory cue with a footshock increases the rate of spine elimination in mouse frontal association *** contrast,fear extinction by repeated presentation of the same auditory cue increases the rate of spine ***,spine elimination and formation induced by fear conditioning and extinction occur on the same dendritic branches in a cue-and location-specific ***,reconditioning preferentially induces elimination of dendritic spines that were formed after ***,within vastly complex neuronal networks,fear conditioning,extinction and reconditioning lead to opposing changes at the level of individual *** recently found that this opposing dendritic spine plasticity was also observed in primary auditory *** findings suggest that fear memory trace erasure could be a universal phenomenon in neocortex after fear extinction.

关键词： Fear conditioning dendritic spine Plasticity Frontal association cortex Auditory cortex

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Calsyntenin-1 Implicates in dendritic spine Abnormalities in Fragile X Syndrome Mouse Model by Modulating dendritic ICAM5 Redistribution

Calsyntenin-1 Implicates in Dendritic Spine Abnormalities in...

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中国神经科学学会第十二届全国学术会议

作者： Ke Cheng Yan Zeng Qiong Zhu Zhi-wei Zhang Gui-rong Cheng Dan Liu Brain and Cognitive Function Laboratory Wuhan University of Science and Technology

Objective Our prior studies have demonstrated the critical role of the neuronspecific intercellular adhesion molecule 5（ICAM5, telencephalin） in spine development and revealed its implication in the dendritic spine maturation of fragile X syndrome（FXS）. But, the molecular mechanism that results in ICAM5 dysregulation in FXS has not been studied yet. The present study is to explore the role of calsyntenin-1（Clstn1）, type-1 transmembrane proteins of the cadherin superfamily, in spine maturation in FXS neurons, and whether it mediates intracellular transportation of ICAM5 and redistribution. Methods Fmr1 knock out（KO）（FVB 129 P2-Pde6 b+ Tyrc-ch-Fmr1 tm1 Cgr/J） and control（FVB.129 P2-Pde6 b Tyrc-ch/Ant J）, here-after referred to as wild-type（WT） strain mice were used as the animal model of FXS. Primary mouse neuronal cultures were generated from prefrontal cerebral cortex of WT or Fmr1-KO embryos（E17–E18）. The interaction between Clstn1 and Icam5 was identified by live cell imaging and time-lapse analysis, immunocytochemistry and colocalization. The alteration of dendritic spine in neurons was measured by confocal analysis. The pattern of postnatal spine development was profiled by Golgi staining. Results（1） Fmr1 KO presented anomalous postnatal dendritic spines that are concomitant to abundant ICAM5 expression and decreased synaptic calsyntenin-1 in a few brain areas.（2） Clstn1 was colocalized with Icam5 in cultured mouse neurons and in N2 a cell line.（3） Clstn1 deletion in neurons resulted in increased expression of Icam5 on membrane and redistribution in neurons, while reexpression of Clstn1 normalized Icam5 distribution.（4） Clstn1 deletion in neurons resulted in decreased dendritic arborization and increased proportions of immature filopodia-like dendritic protrusions, while re-expression of Clstn1 rescued the spine retraction response. Conclusion Clstn1 mediates ICAM5 redistribution, and further promotes spine maturation. In its dysregulation in Fmr1 KO mice, the f

关键词： Calsyntenin-1 intercellular adhesion molecule-5 dendritic spine intracellular transport Fragile X syndrome

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The FMRP/ICAM5 mRNA Interaction Uncovers a New Mechanism of Modulating dendritic spine Development and Cognitive Behaviors in Fragile X Syndrome

The FMRP/ICAM5 mRNA Interaction Uncovers a New Mechanism of ...

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中国神经科学学会第十二届全国学术会议

作者： Ya-Ping Pei Yan Zeng Shi-jing Yuan Mi Tian Lang Xu Qiong Zhu Ming-Gao Zhao Brain and Cognitive Function Laboratory Wuhan University of Science and Technology

Objective Fragile X syndrome（FXS） is the most common cause of intellectual disability in males and the most common single gene cause of autism. Dendrite and spine abnormalities have been correlated with impaired cognitive abilities in FXS, where neurons show a high density of long, thin, and immature dendritic spines. But the causes of these malformations are not yet well understood. Intercellular adhesion molecule 5（ICAM5;Telencephalin）, a protein of the Ig superfamily, has been implicated in neuronal and spine development as well as the formation and maintenance of dendritic filopodia. The present study is to examine a possible link for ICAM5 in Fmr1 knockout（KO） mice, the animal model of FXS and to futher investigate the direct interaction of FMRP and ICAM5. Methods Fmr1 knock out（KO）（FVB 129 P2-Pde6 b+Tyrc-ch-Fmr1 tm1 Cgr/J） and control（FVB.129 P2-Pde6 b Tyrc-ch/Ant J）, here-after referred to as wild-type（WT） strain mice were used as the animal model of FXS. Primary mouse neuronal cultures were generated from prefrontal cerebral cortex of WT or Fmr1-KO embryos（E17–E18）. The pattern of postnatal spine development and ICAM5 expression was profiled by Golgi staining and western blot respectively. The interaction between Clstn1 and Icam5 m RNA was identified by RNA binding protein immunoprecipitation and quantitative real-time PCR. The alteration of dendritic spine in neurons was measured by live cell imaging. Results（1） In Fmr1 KO brains and cultured neurons, ICAM5 m RNA translation was enhanced by the loss of FMRP, leading to excessive production of ICAM5 protein and preventing filopodiato-spine transition, but ICAM5 m RNA was less affected.（2） Genetic reduction of ICAM5 by using si RNA ICAM5 normalized the aberrant spine maturation and ameliorated behavior impairments including spatial and fear memory in Fmr1 KO mice.（3） FMRP was immunoprecipitated with ICAM5 m RNA from mouse brain and the binding region in ICAM5 was localized to the two first Ig domains. Conclus

关键词： Fragile X syndrome fragile X mental retardation protein intercellular adhesion molecule-5 dendritic spine interaction

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Initiation of dendritic NMDA spikes co-regulated via distance-dependent and dynamic distribution of the spine number and morphology in neuron dendrites

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Science China(Technological Sciences) 2023年第2期66卷 429-438页

作者： CAO YuWei SHEN Chun QIU Hu GUO WanLin State Key Laboratory of Tribology Department of Mechanical EngineeringTsinghua UniversityBeijing 100084China State Key Laboratory of Mechanics and Control of Mechanical Structure and Key Laboratory for Intelligent Nano Materials and Devices of the Ministry of Education Institute for Frontier Science and Institute of NanoscienceNanjing University of Aeronautics and AstronauticsNanjing 210016China

dendritic spines are small membranous protrusions that receive synaptic inputs from other neurons,enabling the initiation of dendritic N-methyl-D-aspartic(NMDA)spikes and somatic action *** learning and memory processes,both the number of spines on a dendrite and the morphology of individual spines are constantly *** individual influence of spine number and morphology on dendritic NMDA spikes has already been revealed,but the functional significance of the coregulation of spine number and morphology on NMDA spikes remains ***,we systematically investigated the initiation of local dendritic NMDA spikes by the dynamic distributions of the spine number and morphology on single dendrites in reconstructed neuron *** from the traditional cognition,we found the threshold number of spines required to generate local dendrite NMDA spikes on distal dendrites is fewer than that on proximal ones,because the thinner distal dendrites own higher *** for the spine morphology,the presence of moreα-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid(AMPA)receptors on the spine leads to larger NMDA spikes rather than an increase in the spine dimension ***,we first suggested that a single dendrite containing spines with gradually increasing head diameters away from the soma could generate larger NMDA spikes than that irrational distribution of spine morphology containing spines with decreasing head diameters,which can be compensated by the increasing spine ***,the distance-dependent distribution of spine number and morphology co-regulate the intension of dendritic NMDA *** findings about the threshold for NMDA spikes provide novel insights into the role of the irrational dynamic distribution of the spine number and morphology in senescence and disease processes such as Alzheimer’s disease,schizophrenia,and Parkinson’s disease,which causes abnormal neuron firing.

关键词： dendritic spine spine number spine morphology NMDA spikes memory neurological diseases

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Treadmill Exercise Reshapes Cortical Astrocytic and Neuronal Activity to Improve Motor Learning Deficits Under Chronic Alcohol Exposure

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Neuroscience Bulletin 2024年第9期40卷 1287-1298页

作者： Linglin Liu Lanzhi Luo Ji-an Wei Xintong Xu Kwok-Fai So Li Zhang Key Laboratory of CNS Regeneration(Ministry of Education) Guangdong-Hong Kong-Macao Institute of CNS RegenerationJinan UniversityGuangzhou510632China College of Life Science and Technology Jinan UniversityGuangzhou510632China State Key Laboratory of Brain and Cognitive Science Li Ka Shing Faculty of MedicineThe University of Hong KongPok Fu LamHong Kong SARChina Neuroscience and Neurorehabilitation Institute University of Health and Rehabilitation SciencesQingdao266113China Center for Exercise and Brain Science School of PsychologyShanghai University of SportShanghai200438China The First Affiliated Hospital of Xinxiang Medical University Xinxiang453003China

Alcohol abuse induces various neurological disorders including motor learning deficits,possibly by affecting neuronal and astrocytic *** exercise is one effective approach to remediate synaptic loss and motor deficits as shown by our previous *** this study,we unrevealed the role of exercise training in the recovery of cortical neuronal and astrocytic *** a chronic alcohol injection mouse model,we found the hyperreactivity of astrocytes along with dendritic spine loss plus lower neuronal activity in the primary motor *** treadmill exercise training,on the other hand,improved neural spine formation and inhibited reactive astrocytes,alleviating motor learning deficits induced by alcohol *** data collectively support the potency of endurance exercise in the rehabilitation of motor functions under alcohol abuse.

关键词： Alcohol abuse Motor learning dendritic spine Reactive astrocyte

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Fasting produces antidepressant-like effects via activating mammalian target of rapamycin complex 1 signaling pathway in ovariectomized mice

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Neural Regeneration Research 2023年第9期18卷 2075-2081页

作者： Zi-Qian Cheng Jie Fan Fang-Yi Zhao Jing-Yun Su Qi-Han Sun Ran-Ji Cui Bing-Jin Li Jilin Provincial Key Laboratory on Molecular and Chemical Genetic The Second Hospital of Jilin UniversityChangchunJilin ProvinceChina Jilin Engineering Laboratory for Screening of Antidepressant ChangchunJilin ProvinceChina

Recent studies have shown that a 9-hour fast in mice reduces the amount of time spent immobile in the forced swimming *** r,whether 9-hour fasting has therapeutic effects in female mice with depressive symptoms has not been ***,in this study,we simulated perimenopausal depression via an ovariectomy in mice,and subjected them to a single 9-hour fasting 7 days *** found that the ovariectomy increased the time spent immobile in the forced swimming test,inhibited expression of the mammalian target of rapamycin complex 1 signaling pathway in the hippocampus and prefro ntal cortex,and decreased the density of dendritic spines in the *** 9-hour acute fasting alleviated the above-mentioned ***,all of the antidepressant-like effects of 9-hour fasting were reve rsed by an inhibitor of the mammalian to rget of rapamycin complex *** data showed a remarkable increase in long-term potentiation in the hippocampal CA1 of the ovariectomized mice subjected to fasting compared with the findings in the ovariectomized mice not subjected to *** findings show that the antidepressant-like effects of 9-hour fasting may be related to the activation of the mammalian target of the rapamycin complex 1 signaling pathway and synaptic plasticity in the mammalian ***,fasting may be a potential treatment for depression.

关键词： antidepressant brain-derived neurotrophic factor dendritic spine fasting hippocampus LTP mTOR complex 1 neural plasticity ovariectomized mice rapamycin

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Blunt dopamine transmission due to decreased GDNF in the PFC evokes cognitive impairment in Parkinson’s disease

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Neural Regeneration Research 2023年第5期18卷 1107-1117页

作者： Chuan-Xi Tang Jing Chen Kai-Quan Shao Ye-Hao Liu Xiao-Yu Zhou Cheng-Cheng Ma Meng-Ting Liu Ming-Yu Shi Piniel Alphayo Kambey Wei Wang Abiola Abdulrahman Ayanlaja Yi-Fang Liu Wei Xu Gang Chen Jiao Wu Xue Li Dian-Shuai Gao Department of Neurobiology Xuzhou Key Laboratory of NeurobiologyXuzhou Medical UniversityXuzhouJiangsu ProvinceChina Experinental Teaching Center of Morphology Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Neurology Affiliated Suqian Hospital of Xuzhou Medical UniversitySuqianJiangsu ProvinceChina Department of Rehabilitation Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Neurology Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Medicine Jiangnan UniversityWuxiJiangsu ProvinceChina Department of Nursing Care the Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina

Studies have found that the absence of glial cell line-derived neurotrophic factor may be the primary risk factor for Parkinson’s disease. However, there have not been any studies conducted on the potential relationship between glial cell line-derived neurotrophic factor and cognitive performance in Parkinson’s disease. We first performed a retrospective case-control study at the Affiliated Hospital of Xuzhou Medical University between September 2018 and January 2020 and found that a decreased serum level of glial cell line-derived neurotrophic factor was a risk factor for cognitive disorders in patients with Parkinson’s disease. We then established a mouse model of Parkinson’s disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and analyzed the potential relationships among glial cell line-derived neurotrophic factor in the prefrontal cortex, dopamine transmission, and cognitive function. Our results showed that decreased glial cell line-derived neurotrophic factor in the prefrontal cortex weakened dopamine release and transmission by upregulating the presynaptic membrane expression of the dopamine transporter, which led to the loss and primitivization of dendritic spines of pyramidal neurons and cognitive impairment. In addition, magnetic resonance imaging data showed that the long-term lack of glial cell line-derived neurotrophic factor reduced the connectivity between the prefrontal cortex and other brain regions, and exogenous glial cell line-derived neurotrophic factor significantly improved this connectivity. These findings suggested that decreased glial cell line-derived neurotrophic factor in the prefrontal cortex leads to neuroplastic degeneration at the level of synaptic connections and circuits, which results in cognitive impairment in patients with Parkinson’s disease.

关键词： cognitive impairment degree centrality dendritic spine dopamine transmission dopamine transporter glial cell line-derived neurotrophic factor Parkinson’s disease prefrontal cortex synaptic plasticity

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