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A review of the neurotransmitter system associated with cognitive function of the cerebellum in Parkinson's disease

Neural Regeneration Research 2024年第2期19卷 324-330页

作者： Xi Chen Yuhu Zhang Department of Neurology Guangdong Neuroscience InstituteGuangdong Provincial People’s Hospital(Guangdong Academy of Medical Sciences)Southern Medical UniversityGuangzhouGuangdong ProvinceChina Shantou University Medical College ShantouGuangdong ProvinceChina

The dichotomized brain system is a concept that was generalized from the‘dual syndrome hypothesis’to explain the heterogeneity of cognitive impairment,in which anterior and posterior brain systems are independent but partially overlap.The dopaminergic system acts on the anterior brain and is responsible for executive function,working memory,and planning.In contrast,the cholinergic system acts on the posterior brain and is responsible for semantic fluency and visuospatial function.Evidence from dopaminergic/cholinergic imaging or functional neuroimaging has shed significant insight relating to the involvement of the cerebellum in the cognitive process of patients with Parkinson’s disease.Previous research has reported evidence that the cerebellum receives both dopaminergic and cholinergic projections.However,whether these two neurotransmitter systems are associated with cognitive function has yet to be fully elucidated.Furthermore,the precise role of the cerebellum in patients with Parkinson’s disease and cognitive impairment remains unclear.Therefore,in this review,we summarize the cerebellar dopaminergic and cholinergic projections and their relationships with cognition,as reported by previous studies,and investigated the role of the cerebellum in patients with Parkinson’s disease and cognitive impairment,as determined by functional neuroimaging.Our findings will help us to understand the role of the cerebellum in the mechanisms underlying cognitive impairment in Parkinson’s disease.

关键词： anterior brain system cerebellum cholinergic cognitive impairment dopaminergic dual syndrome hypothesis neuroimage neurotransmitter Parkinson’s disease posterior brain system therapeutic targets

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Tetrabromobisphenol A exerts thyroid disrupting effects but has little overt impact on postnatal brain development and neurobehaviors in mice

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Journal of Environmental Sciences 2024年第8期142卷 1-10页

作者： Shilin Song Yuanyuan Li Lin Lv Mengqi Dong Zhanfen Qin State Key Laboratory of Environmental Chemistry and Ecotoxicology Research Center for Eco-Environmental SciencesChinese Academy of SciencesBeijing 100085China College of Resources and Environment University of Chinese Academy of SciencesBeijing 100049China School of Environment Tsinghua UniversityBeijing 100084China

Tetrabromobisphenol A(TBBPA)is a widely used brominated flame retardant.There is evidence showing that TBBPA can exert thyroid disrupting effects in mammals,but different results were also reported,along with inconsistent reports regarding its neurotoxicity.Here,we investigated thyroid disrupting effects and neurotoxicity of TBBPA(5,50,500μg/(kg·day))to male mice following maternal and direct exposure through drinking water,with the antithyroid drug propylthiouracil(PTU)as the positive control.On postnatal day(PND)15,we expectedly observed severe thyroid compensatory hyperplasia and cerebellar developmental retardation in PTU-treated pups.The highest dose of TBBPA also caused thyroid histological alteration but had no effects on cerebellar development in terms of Purkinje cell morphology and the thickness of the internal granular layer and the molecular layer of the cerebellum.During puberty and adulthood,the thyroid morphological alterations became more pronounced in the TBBPA-treated animals,accompanied by decreased serum thyroid hormone levels.Furthermore,the 50 and 500μg/(kg·day)TBBPA groups showed a significant decrease in the serum level of serotonin,a neurotransmitter associated with anxiety behaviors.Correspondingly,the highest dose group displayed anxiety-like behaviors in the elevated plus-maze test on PND 35,but this neurobehavioral alteration disappeared on PND 56.Moreover,no changes in neurobehavioral parameters tested were found in TBBPAtreated animals at puberty and adulthood.Altogether,all observations show that TBBPA can exert thyroid disrupting effects but has little overt impact on brain development and neurobehaviors in mice,suggesting that thyroid disruption does not necessarily cause overtly adverse neurodevelopmental outcomes.

关键词： Tetrabromobisphenol A Thyroid disruption Brain development Neurobehavior cerebellum

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Exploring cerebral structural and functional abnormalities in a mouse model of post-traumatic headache induced by mild traumatic brain injury

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Zoological Research 2024年第3期45卷 648-662页

作者： Dan Yang Bin-Bin Nie Jin-Gang He Zong-Qiang Lv Feng-Feng Mo Si-Yi Ouyang Jie Wang Ju-Xiang Chen Tao Tao Department of Anesthesiology Central People’s Hospital of ZhanjiangZhanjiangGuangdong 524045China Key Laboratory of Nuclear Radiation and Nuclear Energy Technology Institute of High Energy PhysicsChinese Academy of SciencesBeijing 100049China Key Laboratory of Magnetic Resonance in Biological Systems State Key Laboratory of Magnetic Resonance and Atomic and Molecular PhysicsNational Center for Magnetic Resonance in WuhanWuhan Institute of Physics and MathematicsInnovation Academy for Precision Measurement Science and TechnologyChinese Academy of Sciences-Wuhan National Laboratory for OptoelectronicsWuhanHubei 430071China Department of Neurosurgery Changhai HospitalNaval Medical UniversityShanghai 200082China Department of Nutrition and Food Hygiene Faculty of Naval MedicineNaval Medical UniversityShanghai 200433China Department of Anesthesiology Nanfang HospitalSouthern Medical UniversityGuangzhouGuangdong 510515China Institute of Neuroscience and Brain Diseases/Xiangyang Central Hospital Affiliated Hospital of Hubei University of Arts and ScienceXiangyangHubei 441021China Songjiang Hospital and Songjiang Research Institute Shanghai Jiao Tong University School of MedicineShanghai 201600China Department of Anesthesiology Zhujiang HospitalSouthern Medical UniversityGuangzhouGuangdong 510515China

Mild traumatic brain injury(mTBI)-induced post-traumatic headache(PTH)is a pressing public health concern and leading cause of disability worldwide.Although PTH is often accompanied by neurological disorders,the exact underlying mechanism remains largely unknown.Identifying potential biomarkers may prompt the diagnosis and development of effective treatments for mTBI-induced PTH.In this study,a mouse model of mTBI-induced PTH was established to investigate its effects on cerebral structure and function during short-term recovery.Results indicated that mice with mTBI-induced PTH exhibited balance deficits during the early post-injury stage.Metabolic kinetics revealed that variations in neurotransmitters were most prominent in the cerebellum,temporal lobe/cortex,and hippocampal regions during the early stages of PTH.Additionally,variations in brain functional activities and connectivity were further detected in the early stage of PTH,particularly in the cerebellum and temporal cortex,suggesting that these regions play central roles in the mechanism underlying PTH.Moreover,our results suggested that GABA and glutamate may serve as potential diagnostic or prognostic biomarkers for PTH.Future studies should explore the specific neural circuits involved in the regulation of PTH by the cerebellum and temporal cortex,with these two regions potentially utilized as targets for non-invasive stimulation in future clinical treatment.

关键词： Post-traumatic headache(PTH) Mild traumatic brain injury(mTBI) Metabolic kinetics fMRI cerebellum

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Sequential stabilization of RNF220 by RLIM and ZC4H2 during cerebellum development and Shh-group medulloblastoma progression

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Journal of Molecular Cell Biology 2022年第1期14卷 32-46页

作者： Yuwei Li Chencheng Yang Huishan Wang Ling Zhao Qinghua Kong Yu Cang Shuhua Zhao Longbao Lv Yan Li Bingyu Mao Pengcheng Ma State Key Laboratory of Genetic Resources and Evolution Kunming Institute of ZoologyChinese Academy of SciencesKunming 650223China Kunming College of Life Science University of Chinese Academy of SciencesKunming 650203China Experimental Animal Center Kunming Institute of ZoologyChinese Academy of SciencesKunming 650223China Kunming Institute of Botany Chinese Academy of SciencesKunming 650223China Department of Urology the Affiliated Hospital of Yunnan UniversityKunming 650021China First Affiliated Hospital of Kunming Medical University Kunming 650032China Center for Excellence in Animal Evolution and Genetics Chinese Academy of SciencesKunming 650223China

Sonic hedgehog (Shh) signaling is essential for the proliferation of cerebellar granule neuron progenitors (CGNPs), and its misregulation is linked to various disorders, including cerebellar cancer medulloblastoma (MB). During vertebrate neural development, RNF220, a ubiquitin E3 ligase, is involved in spinal cord patterning by modulating the subcellular location of glioma-associated oncogene homologs (Glis) through ubiquitination. RNF220 is also required for full activation of Shh signaling during cerebellum development in an epigenetic manner through targeting embryonic ectoderm development. ZC4H2 was reported to be involved in spinal cord patterning by acting as an RNF220 stabilizer. Here, we provided evidence to show that ZC4H2 is also required for full activation of Shh signaling in CGNP and MB progression by stabilizing RNF220. In addition, we found that the ubiquitin E3 ligase RING finger LIM domain-binding protein (RLIM) is responsible for ZC4H2 stabilization via direct ubiquitination, through which RNF220 is also thus stabilized. RLIM is a direct target of Shh signaling and is also required for full activation of Shh signaling in CGNP and MB cell proliferation. We further provided clinical evidence to show that the RLIM‒ZC4H2‒RNF220 cascade is involved in Shh-group MB progression. Disease-causative human RLIM and ZC4H2 mutations affect their interaction and regulation. Therefore, our study sheds light on the regulation of Shh signaling during cerebellar development and MB progression and provides insights into neural disorders caused by RLIM or ZC4H2 mutations.

关键词： ZC4H2 RLIM RNF220 Shh signaling cerebellum medulloblastoma(MB)

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Cerebellar pathology in motor neuron disease:neuroplasticity and neurodegeneration

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Neural Regeneration Research 2022年第11期17卷 2335-2341页

作者： Rangariroyashe H.Chipika Grainne Mulkerrin Pierre-François Pradat Aizuri Murad Fabrice Ango Cédric Raoul Peter Bede Computational Neuroimaging Group Biomedical Sciences InstituteTrinity College DublinDublinIreland Pitié-Salpêtrière University Hospital Sorbonne UniversityParisFrance The Neuroscience Institute of Montpellier(INM) INSERMCNRSMontpellierFrance

Amyotrophic lateral sclerosis is a relentlessly progressive multi-system condition.The clinical picture is dominated by upper and lower motor neuron degeneration,but extra-motor pathology is increasingly recognized,including cerebellar pathology.Post-mortem and neuroimaging studies primarily focus on the chara cterization of supratentorial disease,des pite emerging evidence of cerebellar degeneration in amyotrophic lateral sclerosis.Cardinal clinical features of amyotrophic lateral sclerosis,such as dysarthria,dysphagia,cognitive and behavioral deficits,saccade abnormalities,gait impairment,respiratory weakness and pseudobulbar affect are likely to be exacerbated by co-existing cerebellar pathology.This review summarizes in vivo and post mortem evidence for cerebellar degeneration in amyotrophic lateral scle rosis.Structural imaging studies consistently capture cerebellar grey matter volume reductions,diffusivity studies readily detect both intra-cerebellar and cerebellar peduncle white matter alte rations and functional imaging studies commonly report increased functional connectivity with supratentorial regions.Increased functional connectivity is commonly interpreted as evidence of neuro plasticity representing compensatory processes despite the lack of post-mortem validation.There is a scarcity of post-mortem studies focusing on cerebellar alte rations,but these detect pTDP-43 in cerebellar nuclei.Ce rebellar pathology is an overloo ked facet of neurodegeneration in amyotrophic lateral sclerosis despite its contribution to a multitude of clinical symptoms,wides p read connectivity to spinal and supratentorial regions and putative role in compensating for the degeneration of primary motor regions.

关键词： amyotrophic lateral sclerosis ataxia cerebellum magnetic resonance imaging motor neuron disease neuroimaging neuroplasticity pathology primary lateral sclerosis pseudobulbar affect

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Deletion of CHD8 in cerebellar granule neuron progenitors leads to severe cerebellar hypoplasia,ataxia,and psychiatric behavior in mice

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Journal of Genetics and Genomics 2022年第9期49卷 859-869页

作者： Xiang Chen Tong Chen Chen Dong Huiyao Chen Xinran Dong Lin Yang Liyuan Hu Huijun Wang Bingbing Wu Ye Yao Yu Xiong Man Xiong Yifeng Lin Wenhao Zhou Departments of Neonatology Children's Hospital of Fudan UniversityNational Children's Medical CenterShanghai201102China Institutes of Biomedical Sciences Fudan UniversityShanghai200032China Key Laboratory of Birth Defects Children's Hospital of Fudan UniversityNational Children's Medical CenterShanghai201102China Department of Biostatistics School of Public HealthFudan UniversityShanghai200032China Department of Obstetrics Obstetrics and Gynecology Hospital of Fudan UniversityShanghai200090China Stem Cell Center Children's Hospital of Fudan UniversityShanghai201102China MOE Frontiers Center for Brain Science Fudan UniversityShanghai201102China

CHD8 is a candidate gene for autism spectrum disorders and neurological development delay.It has been reported to be essential for neurogenesis in the cerebral cortex,but the function of CHD8 in cerebellum has not been comprehensively investigated.The potential relationship of cerebellum dysplasia with psychiatric disorders in patients with CHD8 mutations is still not clear.In this study,we establish different conditional knockout mouse models to investigate the roles of CHD8 in cerebellar development.Mice with neural stem cell-specific Chd8 deletion exhibit significant reduction of cerebellum volume and no layering structure is detected.Genetic deletion of Chd8 in cerebellar granule neuron progenitors(GNPs)leads to cerebellar hypoplasia,absent of proliferation layer and ectopic of Purkinje neuron.However,no substantial cerebellar dysplasia is detected in mice with Purkinje neuron-or oligodendrocyte-specific Chd8 ablation.Single-cell RNA sequencing indicates that ribosome-related genes and pathways are most significantly disrupted in GNPs,indicating the potential mechanism.Importantly,in addition to the ataxia phenotype,mice with GNPspecific Chd8 ablation present a neuropsychiatric phenotype in three-chamber and light/dark tests.Taken together,our results provide insights not only into the function of CHD8 in cerebellar development,but also the pathogenesis of neuropsychiatric disorders in patients with CHD8 mutations.

关键词： cerebellum Granule neuron CHD8 Autism spectrum disorder

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Ataxia-telangiectasia mutated plays an important role in cerebellar integrity and functionality

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Neural Regeneration Research 2023年第3期18卷 497-502页

作者： Yulia Mitiagin Ari Barzilai Department of Neurobiology the School of NeurobiologyBiophysicsMolecular Biology and BiochemistryGeorge S.WiseFaculty of Life SciencesTel Aviv UniversityTel AvivIsrael Sagol School of Neurosciences Tel Aviv UniversityTel AvivIsrael

Accumulating evidence indicates that ataxia-telangiectasia mutated kinase is critical for maintaining cellular homeostasis and that it has both nuclear and cytoplasmic functions.However,the functions of ataxia-telangiectasia mutated that when lost lead to cerebellar degeneration are still unknown.In this review,we first describe the role of ataxia-telangiectasia mutated in cerebellar pathology.In addition to its canonical nuclear functions in DNA damage response circuits,ataxia-telangiectasia mutated functions in various cytoplasmic and mitochondrial processes that are critically important for cellular homeostasis.We discuss these functions with a focus on the role of ataxia-telangiectasia mutated in maintaining the homeostatic redox state.Finally,we describe the unique functions of ataxia-telangiectasia mutated in various types of neuronal and glial cells including cerebellar granule neurons,astrocytes,and microglial cells.

关键词： ataxia telangiectasia ATM cerebellum DNA damage response double-strand breaks mitochondrial dysfunction oxidative stress single-strand breaks

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Cre-recombinase systems for induction of neuronspecific knockout models:a guide for biomedical researchers

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Neural Regeneration Research 2023年第2期18卷 273-279页

作者： Tetiana Shcholok Eftekhar Eftekharpour Spinal Cord Research Centre Department of Physiology and PathophysiologyUniversity of ManitobaWinnipegMBCanada

Gene deletion has been a valuable tool for unraveling the mysteries of molecular biology.Early approaches included gene trapping and gene targetting to disrupt or delete a gene randomly or at a specific location,respectively.Using these technologies in mouse embryos led to the generation of mouse knocko ut models and many scientific discoveries.The efficacy and specificity of these approaches have significantly increased with the advent of new technology such as cluste red regula rly inters paced short palindromic repeats for targetted gene deletion.However,several limitations including unwanted off-target gene deletion have hindered their widespread use in the field.Crerecombinase technology has provided additional capacity for cell-specific gene deletion.In this review,we provide a summary of currently available literature on the application of this system for targetted deletion of neuronal genes.This article has been constructed to provide some background info rmation for the new trainees on the mechanism and to provide necessary information for the design,and application of the Cre-recombinase system thro ugh reviewing the most f requent promoters that are currently available for genetic manipulation of neuro ns.We additionally will provide a summary of the latest technological developments that can be used for targeting neurons.This may also serve as a general guide for the selection of appropriate models for biomedical research.

关键词： central nervous system cerebellum Cre/LoxP system Cre-recombinase transduction gene deletion gene delivery hippocampus in vivo genome editing stereotaxic injection

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Heat stroke alters hippocampal and cerebellar transmitter metabonomics

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World Journal of Emergency Medicine 2023年第4期14卷 287-293页

作者： Guoxin He Ancong Xu Xichong Yu Fan Huang Lei Su The First School of Clinical Medicine Southern Medical UniversityGuangzhou 510515China Department of Critical Care Medicine the Third Affiliated Hospital of Wenzhou Medical UniversityWenzhou 325000China School of Pharmaceutical Sciences Wenzhou Medical UniversityWenzhou 325035China

BACKGROUND:The mechanisms underlying heat stroke(HS)-induced hippocampal injury remain unclear.This study aimed to evaluate the HS-induced metabonomics of hippocampal and cerebellar transmitters.METHODS:The HS model was established with male Sprague-Dawley rats subjected to heat exposure of up to 42℃ at a humidity of(55.0±5.0)%.The hippocampal and cerebellar transmitters and metabolites of rats were tested via ultra-high-performance liquid chromatography–mass spectrometry(UPLC-MS/MS).The primary transmitters and metabolites were identified by principal component analysis(PCA)and orthogonal partial least square-discriminant analysis(OPLS-DA).The major metabolic pathways for HS were selected after enrichment.The brain injury was evaluated by histological tests.RESULTS:HS induced hippocampal and cerebellar injuries in rats.HS upregulated the protein levels of hippocampal glutamate,glutamine,gamma-aminobutyric acid,L-tryptophan(Trp),5-hydroxy-indoleacetic acid,and kynurenine;however,it downregulated asparagine,tryptamine,5-hydroxytryptophan,melatonin,3,4-dihydroxyphenylalanine(L-DOPA),and vanillylmandelic acid.HS also sharply elevated the protein levels of cerebellar methionine and Trp,and decreased the levels of serotonin,L-alanine,L-asparagine,L-aspartate,cysteine,norepinephrine,spermine,spermidine,and tyrosine.Hippocampal glutamate,monoamine transmitters,cerebellar aspartate acid,and catecholamine transmitters’metabolic pathways were identified as the main metablic pathways in HS.CONCLUSION:The hippocampus and cerebellum were injured in rats with HS,possibly induced the disorder of hippocampal glutamate and serotonin metabolism,cerebellar aspartate acid and catecholamine transmitter metabolism,and related metabolic pathways.

关键词： Heat stroke Transmitters Rat Hippocampus cerebellum Metabonomics

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Loss of Wtap results in cerebellar ataxia and degeneration of Purkinje cells

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Journal of Genetics and Genomics 2022年第9期49卷 847-858页

作者： Yeming Yang Guo Huang Xiaoyan Jiang Xiao Li Kuanxiang Sun Yi Shi Zhenglin Yang Xianjun Zhu The Sichuan Provincial Key Laboratory for Human Disease Gene Study and Department of Laboratory Medicine Center for Medical GeneticsSichuan Provincial People’s HospitalUniversity of Electronic Science and Technology of ChinaChengduSichuan 610072China Research Unit for Blindness Prevention of Chinese Academy of Medical Sciences(2019RU026) Sichuan Academy of Medical Sciences and Sichuan Provincial People’s HospitalChengduSichuan 610072China Key Laboratory of Tibetan Medicine Research Chinese Academy of Sciences and Qinghai Provincial Key Laboratory of Tibetan Medicine ResearchNorthwest Institute of Plateau BiologyXiningQinghai 810008China

N^(6)-methyladenosine(m^(6)A)modification,which is achieved by the METTL3/METTL14/WTAP methyltransferase complex,is the most abundant internal mRNA modification.Although recent evidence indicates that m^(6)A can regulate neurodevelopment as well as synaptic function,the roles of m^(6)A modification in the cerebellum and related synaptic connections are not well established.Here,we report that Purkinje cell(PC)-specific WTAP knockout mice display early-onset ataxia concomitant with cerebellar atrophy due to extensive PC degeneration and apoptotic cell death.Loss of Wtap also causes the aberrant degradation of multiple PC synapses.WTAP depletion leads to decreased expression levels of METTL3/14 and reduced m^(6)A methylation in PCs.Moreover,the expression of GFAP and NF-L in the degenerating cerebellum is increased,suggesting severe neuronal injuries.In conclusion,this study demonstrates the critical role of WTAP-mediated m^(6)A modification in cerebellar PCs,thus providing unique insights related to neurodegenerative disorders.

关键词： N^(6)-methyladenosine Wtap METTL3 METTL14 Purkinje cell Ataxia cerebellum

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