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Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats withα-synucleinopathy

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Neural Regeneration Research 2024年第9期19卷 2057-2067页

作者： Bismark Gatica-Garcia Michael J.Bannon Irma Alicia Martínez-Dávila Luis O.Soto-Rojas David Reyes-Corona Lourdes Escobedo Minerva Maldonado-Berny ME Gutierrez-Castillo Armando J.Espadas-Alvarez Manuel A.Fernandez-Parrilla Juan U.Mascotte-Cruz CP Rodríguez-Oviedo Irais E.Valenzuela-Arzeta Claudia Luna-Herrera Francisco E.Lopez-Salas Jaime Santoyo-Salazar Daniel Martinez-Fong departamento de Fisiología Biofísica y NeurocienciasCentro de Investigación y de Estudios AvanzadosCiudad de MéxicoMéxico department of Pharmacology Wayne State University School of MedicineDetroitMIUSA laboratorio de Patogénesis Molecular Carrera Médico CirujanoFacultad de Estudios Superiores IztacalaUniversidad Nacional Autónoma de MéxicoTlalnepantla de BazMéxico Red de Medicina para la Educación y desarrollo y la Investigación Científica de Iztacala(Red MEDICI) Carrera Médico CirujanoFacultad de Estudios Superiores IztacalaUniversidad Nacional Autónoma de MéxicoTlalnepantla de BazMéxico Nanoparticle Therapy Institute AguascalientesMéxico departamento de Biociencias e Ingeniería Centro Interdisciplinario de Investigaciones y Estudios sobre Medio Ambiente y DesarrolloInstituto Politécnico NacionalCiudad de MéxicoMéxico Escuela Nacional de Medicina y Homeopatía Instituto Politécnico NacionalCiudad de MéxicoMéxico departamento de Fisiología Escuela Nacional de Ciencias BiológicasInstituto Politécnico NacionalCiudad de MéxicoMéxico departamento de Biología Molecular y Biotecnología Instituto de Investigaciones BiomédicasUniversidad Nacional Autónoma de MéxicoCiudad de MéxicoMéxico departamento de Física Centro de Investigación y de Estudios AvanzadosCiudad de MéxicoMéxico Programa de Nanociencias y Nanotecnología Centro de Investigación y de Estudios AvanzadosCiudad de MéxicoMéxico

Parkinsonism by unilateral,intranigralβ-sitosterolβ-D-glucoside administration in rats is distinguished in that theα-synuclein insult begins unilaterally but spreads bilaterally and increases in severity over time,thus replicating several clinical features of Parkinson’s disease,a typicalα-synucleinopathy.As Nurr1 repressesα-synuclein,we evaluated whether unilateral transfected of rNurr1-V5 transgene via neurotensin-polyplex to the substantia nigra on day 30 after unilateralβ-sitosterolβ-D-glucoside lesion could affect bilateral neuropathology and sensorimotor deficits on day 30 post-transfection.This study found that rNurr1-V5 expression but not that of the green fluorescent protein(the negative control)reducedβ-sitosterolβ-D-glucoside-induced neuropathology.Accordingly,a bilateral increase in tyrosine hydroxylase-positive cells and arborization occurred in the substantia nigra and increased tyrosine hydroxylase-positive ramifications in the striatum.In addition,tyrosine hydroxylase-positive cells displayed less senescence markerβ-galactosidase and more neuron-cytoskeleton markerβIII-tubulin and brain-derived neurotrophic factor.A significant decrease in activated microglia(positive to ionized calcium-binding adaptor molecule 1)and neurotoxic astrocytes(positive to glial fibrillary acidic protein and complement component 3)and increased neurotrophic astrocytes(positive to glial fibrillary acidic protein and S100 calcium-binding protein A10)also occurred in the substantia nigra.These effects followed the bilateral reduction inα-synuclein aggregates in the nigrostriatal system,improving sensorimotor behavior.Our results show that unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neurodegeneration(senescence and loss of neuron-cytoskeleton and tyrosine hydroxylase-positive cells),neuroinflammation(activated microglia,neurotoxic astrocytes),α-synuclein aggregation,and sensorimotor deficits.Increased neurotrophic astrocytes and brain-derived neurotrophic factor can mediate t

关键词： A1 astrocytes A2 astrocytes gene therapy microglia motor deficits nanoparticles neurodegeneration neuroinflammation senescence α-synuclein aggregates

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Analysis of fluoxetine-induced plasticity mechanisms as a strategy for understanding plasticity related neural disorders

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Neural Regeneration Research 2016年第4期11卷 547-548页

作者： Francesco Mattia Rossi Laboratorio de Neurociencias "Neuroplasticity Unit" Facultad de CienciasUdelaR

Fluoxetine hydrochloride,better known for its commercial name Prozac,is one of the most widely prescribed antidepressant drugs all over the world.This drug was considered a＂breakthrough drug＂for the treatment of depression because of its very high selectivity as a serotonin reuptake inhibitor and because it presented a lower side-effectprofile than previous drugs （Wong et al., 2005）.

关键词： Analysis of fluoxetine-induced plasticity mechanisms as a strategy for understanding plasticity related neural disorders

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Preliminary examination of early neuroconnectivity features in the R6/1 mouse model of Huntington's disease by ultra-high field diffusion MRI

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Neural Regeneration Research 2022年第5期17卷 983-986页

作者： Rodolfo G.Gatto Carina Weissmann department of Bioengineering the University of Illinois at ChicagoChicagoILUSA Instituto de Fisiología Biología Molecular y neurociencias-IFIBYNECONICET Universidad de Buenos AiresBuenos AiresArgentina

During the last decades,advances in the understanding of genetic,cellular,and microstructural alterations associated to Huntington's disease(HD)have improved the understanding of this progressive and fatal illness.However,events related to early neuropathological events,neuroinflammation,deterioration of neuronal connectivity and compensatory mechanisms still remain vastly unknown.Ultra-high field diffusion MRI(UHFD-MRI)techniques can contribute to a more comprehensive analysis of the early microstructural changes observed in HD.In addition,it is possible to evaluate if early imaging microstructural parameters might be linked to histological biomarkers.Moreover,qualitative studies analyzing histological complexity in brain areas susceptible to neurodegeneration could provide information on inflammatory events,compensatory increase of neuroconnectivity and mechanisms of brain repair and regeneration.The application of ultra-high field diffusion-MRI technology in animal models,particularly the R6/1 mice(a common preclinical mammalian model of HD),provide the opportunity to analyze alterations in a physiologically intact model of the disease.Although some disparities in volumetric changes across different brain structures between preclinical and clinical models has been documented,further application of different diffusion MRI techniques used in combination like diffusion tensor imaging,and neurite orientation dispersion and density imaging have proved effective in characterizing early parameters associated to alteration in water diffusion exchange within intracellular and extracellular compartments in brain white and grey matter.Thus,the combination of diffusion MRI imaging techniques and more complex neuropathological analysis could accelerate the discovery of new imaging biomarkers and the early diagnosis and neuromonitoring of patients affected with HD.

关键词： brain repair diffusion tensor imaging Huntington's disease neurite orientation dispersion and density imaging neuroconnectivity neuroinflammation neuroplasticity neuroregeneration R6/1 mice ultra-high field diffusion MRI

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Paternal physical exercise modulates global DNA methylation status in the hippocampus of male rat offspring

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Neural Regeneration Research 2019年第3期14卷 491-500页

作者： Christiano Spindler Ethiane Segabinazi Andre Luis Ferreira de Meireles Francele Valente Piazza Filipe Mega Gabriela dos Santos Salvalaggio Matilde Achaval Viviane Rostirola Elsner Simone Marcuzzo Programa de Pos-Graduacao em neurociencias Instituto de Ciencias Basicas da Saude Universidade Federal do Rio Grande do Sul laboratorio de Histofisiologia Comparada Departamento de Ciencias Morfologicas Instituto de Ciencias Basicas da Saude Universidade Federal do Rio Grande do Sul Programa de Pos-Graduacao em Biociências e Reabilitacao Centro Universitario Metodista-IPA

It is widely known that maternal physical exercise is able to induce beneficial improvements in offspring cognition; however, the effects of paternal exercise have not been explored in detail. The present study was designed to evaluate the impact of paternal physical exercise on memory and learning, neuroplasticity and DNA methylation levels in the hippocampus of male offspring. Adult male Wistar rats were divided into two groups: sedentary or exercised fathers. The paternal preconception exercise protocol consisted of treadmill running, 20 minutes daily, 5 consecutive days per week for 22 days, while the mothers were not trained. After mating, paternal sperm was collected for global DNA methylation analysis. At postnatal day 53, the offspring were euthanized, and the hippocampus was dissected to measure cell survival by 5-bromo-2′-deoxiuridine and to determine the expression of synaptophysin, reelin, brain-derived neurotrophic factor and global DNA methylation levels. To measure spatial memory and learning changes in offspring, the Morris water maze paradigm was used. There was an improvement in spatial learning, as well as a significant decrease in hippocampal global DNA methylation levels in the offspring from exercised fathers compared with those from sedentary ones; however, no changes were observed in neuroplasticity biomarkers brain-derived neurotrophic factor, reelin and 5-bromo-2′-deoxiuridine. Finally, the global DNA methylation of paternal sperm was not significantly changed by physical exercise. These results suggest a link between paternal preconception physical activity and cognitive benefit, which may be associated with hippocampal epigenetic programming in male offspring. However, the biological mechanisms of this modulation remain unclear.

关键词： epigenetics preconception methylation learning treadmill running fetal programming inheritance sperm nerve regeneration

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Physiopathology of ischemic stroke and its modulation using memantine:evidence from preclinical stroke

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Neural Regeneration Research 2021年第3期16卷 433-439页

作者： Hilda Martínez-Coria Isabel Arrieta-Cruz María-Esther Cruz Héctor E.López-Valdés División de Investigación Facultad de MedicinaUniversidad Nacional Autónoma de México(UNAM)Ciudad de MéxicoMéxico laboratorio Experimental de Enfermedades Neurodegenerativas Facultad de MedicinaUNAM/Instituto Nacional de Neurología y NeurocirugíaCiudad de MéxicoMéxico departamento de Investigación Básica Instituto Nacional de GeriatríaCiudad de MéxicoMéxico Unidad de Investigación en Biología de la Reproducción Laboratorio de NeuroendocrinologíaFacultad de Estudios Superiores ZaragozaUNAMCiudad de MéxicoMéxico Unidad Periférica de Neurociencia Facultad de MedicinaUNAM/Instituto Nacional de Neurología y NeurocirugíaCiudad de MéxicoMéxico

Ischemic stroke is the most common type of cerebrovascular disease and is caused by an interruption of blood flow in the brain.In this disease,two different damage areas are identifying:the lesion core,in which cells quickly die;and the penumbra(surrounding the lesion core),in which cells are functionally weakened but may recover and restore their functions.The currently approved treatments for ischemic stroke are the recombinant tissue plasminogen activator and endovascular thrombectomy,but they have a short therapeutic window(4.5 and 6 hours after stroke onset,respectively)and a low percentage of stroke patients actually receive these treatments.Memantine is an approved drug for the treatment of Alzheimer's disease.Memantine is a noncompetitive,low affinity and use-dependent antagonist of N-methyl-D-aspartate glutamate receptor.Memantine has several advantages over developing a new drug to treat focal ischemic stroke,but the most important is that it has sufficient safe probes in preclinical models and humans,and if the preclinical studies provide more evidence about pharmacological actions in tissue protection and repair,this could help to increase the number of clinical trials.The present review summarizes the physiopathology of isquemic stroke and the pharmacological actions in neuroprotection and neuroplasticity of memantine in the post stroke stage of preclinical stroke models,to illustrate their potential to improve functional recovery in human patients.

关键词： focal ischemic stroke memantine neuroplasticity neuroprotection stroke therapy

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Novel TINF2 gene mutation in dyskeratosis congenita with extremely short telomeres:A case report

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World Journal of Clinical Cases 2022年第33期10卷 12440-12446页

作者： Verónica Judith Picos-Cárdenas Saúl Armando Beltrán-Ontiveros JoséAlfonso Cruz-Ramos JoséAlfredo Contreras-Gutiérrez Eliakym Arámbula-Meraz Carla Angulo-Rojo Alma Marlene Guadrón-Llanos Emir Adolfo Leal-León Dora María Cedano-Prieto Juan Pablo Meza-Espinoza laboratorio de Genética Facultad de MedicinaUniversidad Autónoma de SinaloaCuliacán 80018SinaloaMexico Centro de Investigación y Docencia en Ciencias de la Salud Hospital Civil de CuliacánUniversidad Autónoma de SinaloaCuliacán 80030SinaloaMexico departamento de Clínicas Médicas Centro Universitario de Ciencias de la SaludUniversidad de GuadalajaraGuadalajara 44340JaliscoMexico Facultad de Medicina Universidad Autónoma de SinaloaCuliacán 80018SinaloaMexico laboratorio de Genética y Biología Molecular Facultad de Ciencias Químico-BiológicasUniversidad Autónoma de SinaloaCuliacán 80010SinaloaMexico laboratorio de neurociencias Facultad de MedicinaUniversidad Autónoma de SinaloaCuliacán 80018SinaloaMexico laboratorio de Diabetes y Comorbilidades Facultad de MedicinaUniversidad Autónoma de SinaloaCuliacán 80018SinaloaMexico Facultad de Medicina Universidad Autónoma de TamaulipasMatamoros 87349TamaulipasMexico

BACKGROUND Dyskeratosis congenita is a rare disease characterized by bone marrow failure and a clinical triad of oral leukoplakia,nail dystrophy,and abnormal skin pigmentation.The genetics of dyskeratosis congenita include mutations in genes involved in telomere maintenance,including TINF2.CASE SUMMARY Here,we report a female patient who presented thrombocytopenia,anemia,reticulate hyperpigmentation,dystrophy in fingernails and toenails,and leukoplakia on the tongue.A histopathological study of the skin showed dyskeratocytes;however,a bone marrow biopsy revealed normal cell morphology.The patient was diagnosed with dyskeratosis congenita,but her family history did not reveal significant antecedents.Whole-exome sequencing showed a novel heterozygous punctual mutation in exon 6 from the TINF2 gene,namely,NM_001099274.1:-c.854delp.(Val285-Alafs*32).An analysis of telomere length showed short telomeres relative to the patient’s age.CONCLUSION The disease in this patient was caused by a germline novel mutation of TINF2 in one of her parents.

关键词： Dyskeratosis congenita TINF2 Germline mutation Novel mutation Short telomeres Case report

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Melatonin modifies SOX2^+ cell proliferation in dentate gyrus and modulates SIRT1 and MECP2 in long-term sleep deprivation

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Neural Regeneration Research 2019年第10期14卷 1787-1795页

作者： Alan Hinojosa-Godínez Luis F. Jave-Suarez Mario Flores-Soto Alma Y. Gálvez-Contreras Sonia Luquín Edith Oregon-Romero Oscar González-Pérez Rocio E. González-Castaneda laboratorio de Microscopía de Alta Resolución Departamento de NeurocienciasCentro Universitario de Ciencias de la SaludUniversidad de GuadalajaraGuadalajaraMéxico laboratorio de neurociencias Facultad de PsicologíaUniversidad de ColimaColimaMéxico División de Inmunología Centro de Investigación Biomédica de OccidenteInstituto Mexicano del Seguro SocialGuadalajaraMéxico División de neurociencias Centro de Investigación Biomédica de OccidenteInstituto Mexicano del Seguro SocialGuadalajaraMéxico Instituto de Investigación en Ciencias Biomédicas (IICB) Departamento de Biología Molecular y GenómicaCentro Universitario de Ciencias de la SaludUniversidad de GuadalajaraGuadalajaraMéxico Unidad de Atención en neurociencias Departamento de Neurociencias. Centro Universitario de Ciencias de la SaludUniversidad de GuadalajaraGuadalajaraMéxico

Melatonin is a pleiotropic molecule that,after a short-term sleep deprivation,promotes the proliferation of neural stem cells in the adult hippocampus.However,this effect has not been observed in long-term sleep deprivation.The precise mechanism exerted by melatonin on the modulation of neural stem cells is not entirely elucidated,but evidence indicates that epigenetic regulators may be involved in this process.In this study,we investigated the effect of melatonin treatment during a 96-hour sleep deprivation and analyzed the expression of epigenetic modulators predicted by computational text mining and keyword clusterization.Our results showed that the administration of melatonin under sleep-deprived conditions increased the MECP2 expression and reduced the SIRT1 expression in the dentate gyrus.We observed that let-7 b,mir-132,and mir-124 were highly expressed in the dentate gyrus after melatonin administration,but they were not modified by sleep deprivation.In addition,we found more Sox2^+/5-bromo-2’-deoxyuridine(BrdU)^+cells in the subgranular zone of the sleep-deprived group treated with melatonin than in the untreated group.These findings may support the notion that melatonin modifies the expression of epigenetic mediators that,in turn,regulate the proliferation of neural progenitor cells in the adult dentate gyrus under long-term sleep-deprived conditions.All procedures performed in this study were approved by the Animal Ethics Committee of the University of Guadalajara,Mexico(approval No.CI-16610)on January 2,2016.

关键词： sleep-deprivation melatonin microRNA neurogenesis Sirtuin 1 SIRT1 methyl-CpG-binding protein 2 MECP2 epigenetic text-mining mir-9 let-7b

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Cerebral dopamine neurotrophic factor transfection in dopamine neurons using neurotensin-polyplex nanoparticles reverses 6-hydroxydopamine-induced nigrostriatal neurodegeneration

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Neural Regeneration Research 2022年第4期17卷 854-866页

作者： Manuel A.Fernandez-Parrilla David Reyes-Corona Yazmin M.Flores-Martinez Rasajna Nadella Michael J.Bannon Lourdes Escobedo Minerva Maldonado-Berny Jaime Santoyo-Salazar Luis O.Soto-Rojas Claudia Luna-Herrera Jose Ayala-Davila Juan A.Gonzalez-Barrios Gonzalo Flores Maria E.Gutierrez-Castillo Armando JEspadas-Alvarez Irma A.Martínez-Dávila Porfirio Nava Daniel Martinez-Fong departamento de Fisiología Biofísica y NeurocienciasCentro de Investigación y de Estudios AvanzadosCiudad de MéxicoMéxico Programa Institucional de Biomedicina Molecular Escuela Nacional de Medicina y HomeopatíaInstituto Politécnico NacionalCiudad de MéxicoMéxico department of Biosciences IIIT-SrikakulamRajiv Gandhi University of Knowledge Technologies(RGUKT)Andhra PradeshIndia department of Pharmacology Wayne State University School of MedicineDetroitMIUSA departamento de Física Centro de Investigación y de Estudios AvanzadosCiudad de MéxicoMéxico Facultad de Estudios Superiores Iztacala Universidad Nacional Autónoma de MéxicoTlalnepantla de BazEdo.de MéxicoMéxico departamento de Fisiología Escuela Nacional de Ciencias BiológicasCiudad de MéxicoMéxico laboratorio de Medicina Genómica Hospital Regional“1°de Octubre”ISSSTECiudad de MéxicoMéxico laboratorio de Neuropsiquiatría Instituto de FisiologíaBenemérita Universidad Autónoma de PueblaPueblaPueblaMéxico departamento de Biociencias e Ingeniería Centro Interdisciplinario de Investigaciones y Estudios sobre Medio Ambiente y DesarrolloInstituto Politécnico NacionalCiudad de MéxicoMéxico Programa de Nanociencias y nanotecnología Centro de Investigación y de Estudios AvanzadosCiudad de MéxicoMéxico

Overexpression of neurotrophic factors in nigral dopamine neurons is a promising approach to reverse neurodegeneration of the nigrostriatal dopamine system,a hallmark in Parkinson's disease.The human cerebral dopamine neurotrophic factor(h CDNF)has recently emerged as a strong candidate for Parkinson's disease therapy.This study shows that h CDNF expression in dopamine neurons using the neurotensinpolyplex nanoparticle system reverses 6-hydroxydopamine-induced morphological,biochemical,and behavioral alterations.Three independent electron microscopy techniques showed that the neurotensin-polyplex nanoparticles containing the h CDNF gene,ranging in size from 20 to 150 nm,enabled the expression of a secretable h CDNF in vitro.Their injection in the substantia nigra compacta on day 21 after the 6-hydroxydopamine lesion resulted in detectable h CDNF in dopamine neurons,whose levels remained constant throughout the study in the substantia nigra compacta and striatum.Compared with the lesioned group,tyrosine hydroxylase-positive(TH^(+))nigral cell population and TH+fiber density rose in the substantia nigra compacta and striatum after h CDNF transfection.An increase inβIII-tubulin and growth-associated protein 43 phospho-S41(GAP43 p)followed TH^(+)cell recovery,as well as dopamine and its catabolite levels.Partial reversal(80%)of drugactivated circling behavior and full recovery of spontaneous motor and non-motor behavior were achieved.Brain-derived neurotrophic factor recovery in dopamine neurons that also occurred suggests its participation in the neurotrophic effects.These findings support the potential of nanoparticle-mediated h CDNF gene delivery to develop a disease-modifying treatment against Parkinson's disease.The Institutional Animal Care and Use Committee of Centro de Investigación y de Estudios Avanzados approved our experimental procedures for animal use(authorization No.162-15)on June 9,2019.

关键词： axonal growth brain-derived neurotrophic factor gene delivery nanoparticles neuritogenesis neuronal cytoskeleton neuroregeneration neurorestoration neurotrophic therapy Parkinson's disease reinnervation substantia nigra

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The adjustment of γ-aminobutyric acid_A tonic subunits in Huntington＇s disease：from transcription to translation to synaptic levels into the neostriatum

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Neural Regeneration Research 2018年第4期13卷 584-590页

作者： Abraham Rosas-Arellano Argel Estrada-Mondragón Carola A.Mantellero Carlos Tejeda-Guzmán Maite A.Castro Instituto de Bioquimica y Microbiologia Facultad de Ciencias Universidad Austral de Chile Valdivia Chile Center for Interdisciplinary Studies on the Nervous System (CISNe) Universidad Austral de Chile Valdivia Chile departamento de Fisiologla Biofisica y Neurociencias Cinvestav del IPN Ciudad de Mexico Mexico Queensland Brain Institute The University of Queensland Brisbane Australia laboratorio de neurociencias Departamento de Biologia Facultad de Quimica y Biologla Universidad de Santiago de Chile Santiago de Chile Chile

γ-Aminobutyric acid（GABA）,plays a key role in all stages of life,also is considered the main inhibitory neurotransmitter.GABA activates two kind of membrane receptors known as GABAA and GABAB,the first one is responsible to render tonic inhibition by pentameric receptors containing α4-6,β3,δ,or ρ1-3 subunits,they are located at perisynaptic and/or in extrasynaptic regions.The biophysical properties of GABAA tonic inhibition have been related with cellular protection against excitotoxic injury and cell death in presence of excessive excitation.On this basis,GABAA tonic inhibition has been proposed as a potential target for therapeutic intervention of Huntington＇s disease.Huntington＇s disease is a neurodegenerative disorder caused by a genetic mutation of the huntingtin protein.For experimental studies of Huntington＇s disease mouse models have been developed,such as R6/1,R6/2,Hdh Q92,Hdh Q150,as well as YAC128.In all of them,some key experimental reports are focused on neostriatum.The neostriatum is considered as the most important connection between cerebral cortex and basal ganglia structures,its cytology display two pathways called direct and indirect constituted by medium sized spiny neurons expressing dopamine D1 and D2 receptors respectively,they display strong expression of many types of GABAA receptors,including tonic subunits.The studies about of GABAA tonic subunits and Huntington＇s disease into the neostriatum are rising in recent years,suggesting interesting changes in their expression and localization which can be used as a strategy to delay the cellular damage caused by the imbalance between excitation and inhibition,a hallmark of Huntington＇s disease.

关键词： GABAA extrasynaptic and perisynaptic y-aminobutyric acidA receptors striatum R6/1, R6/2,HdhQ92, HdhQ111, HdhQ150, N171-82Q and YAC128 HD transgenics mice models chorea mutanthuntingtin inhibitory neurotransmission D1 medium sized spiny neurons D2 medium sized spiny neurons

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Cerebrospinal fluid and neural stem cell niche control

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Neural Regeneration Research 2018年第9期13卷 1546-1547页

作者： MaIsabel Alonso Angel Gato departamento de Anatomía y Radiología Facultad de MedicinaUniversidad de Valladolid laboratorio de desarrollo y Teratología del Sistema Nervioso Instituto de Neurociencias de Castilla y León (INCYL)Universidad de Valladolid

Neurogenesis from inner brain neural stem cells （NSCs） is a process which takes place continuously in mammals through- out their life. However, the main ontogenic difference is the intensity of neurogenesis, which commences as a very intensive and global activity in the early embryonic brain （neural tube）, persists in fetal and newborn stages, and declines significantly in adulthood, becoming restricted to specific places with low neurogenic activity such as the subventricular zone （SVZ） and the subgranular zone （SGZ） in the dentate gyrus （DG） of the hippocampus.

关键词： SGZ CSF Cerebrospinal fluid and neural stem cell niche control SVZ

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