Development and Evolution of the Human Neocortex
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Suppression of DNA Double-Strand Break Formation by DNA Polymerase B in Active DNA Demethylation Is Required for Development of Hippocampal Pyramidal Neurons
9012 • The Journal of Neuroscience, November 18, 2020 • 40(47):9012–9027 Development/Plasticity/Repair Suppression of DNA Double-Strand Break Formation by DNA Polymerase b in Active DNA Demethylation Is Required for Development of Hippocampal Pyramidal Neurons Akiko Uyeda,1 Kohei Onishi,1 Teruyoshi Hirayama,1,2,3 Satoko Hattori,4 Tsuyoshi Miyakawa,4 Takeshi Yagi,1,2 Nobuhiko Yamamoto,1 and Noriyuki Sugo1 1Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan, 2AMED-CREST, Japan Agency for Medical Research and Development, Suita, Osaka 565-0871, Japan, 3Department of Anatomy and Developmental Neurobiology, Tokushima University Graduate School of Medical Sciences, Kuramoto, Tokushima 770-8503, Japan, and 4Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Aichi 470-1192, Japan Genome stability is essential for brain development and function, as de novo mutations during neuronal development cause psychiatric disorders. However, the contribution of DNA repair to genome stability in neurons remains elusive. Here, we demonstrate that the base excision repair protein DNA polymerase b (Polb) is involved in hippocampal pyramidal neuron fl/fl differentiation via a TET-mediated active DNA demethylation during early postnatal stages using Nex-Cre/Polb mice of ei- ther sex, in which forebrain postmitotic excitatory neurons lack Polb expression. Polb deficiency induced extensive DNA dou- ble-strand breaks (DSBs) in hippocampal pyramidal neurons, but not dentate gyrus granule cells, and to a lesser extent in neocortical neurons, during a period in which decreased levels of 5-methylcytosine and 5-hydroxymethylcytosine were observed in genomic DNA. Inhibition of the hydroxylation of 5-methylcytosine by expression of microRNAs miR-29a/b-1 diminished DSB formation. -
Resting and Active Properties of Pyramidal Neurons in Subiculum and CA1 of Rat Hippocampus
Resting and Active Properties of Pyramidal Neurons in Subiculum and CA1 of Rat Hippocampus NATHAN P. STAFF, HAE-YOON JUNG, TARA THIAGARAJAN, MICHAEL YAO, AND NELSON SPRUSTON Department of Neurobiology and Physiology, Institute for Neuroscience, Northwestern University, Evanston, Illinois 60208 Received 22 March 2000; accepted in final form 8 August 2000 Staff, Nathan P., Hae-Yoon Jung, Tara Thiagarajan, Michael region (Chrobak and Buzsaki 1996; Colling et al. 1998). Sub- Yao, and Nelson Spruston. Resting and active properties of pyrami- iculum has been shown to be the major output center of the dal neurons in subiculum and CA1 of rat hippocampus. J Neuro- hippocampus, to which it belongs, sending parallel projections physiol 84: 2398–2408, 2000. Action potentials are the end product of synaptic integration, a process influenced by resting and active neu- from various subicular regions to different cortical and subcor- ronal membrane properties. Diversity in these properties contributes tical areas (Naber and Witter 1998). Functionally, the principal to specialized mechanisms of synaptic integration and action potential neurons of the subiculum appear to be “place cells,” similar to firing, which are likely to be of functional significance within neural those of CA1 (Sharp and Green 1994); and in a human mag- circuits. In the hippocampus, the majority of subicular pyramidal netic resonance imaging (MRI) study, subiculum was shown to neurons fire high-frequency bursts of action potentials, whereas CA1 be an area involved in memory retrieval (Gabrieli et al. 1997). pyramidal neurons exhibit regular spiking behavior when subjected to Therefore both CA1 and subiculum have been implicated in direct somatic current injection. -
NERVOUS SYSTEM هذا الملف لالستزادة واثراء المعلومات Neuropsychiatry Block
NERVOUS SYSTEM هذا الملف لﻻستزادة واثراء المعلومات Neuropsychiatry block. قال تعالى: ) َو َل َق د َخ َل قنَا ا ِْلن َسا َن ِمن ُس ََل َل ة ِ من ِطي ن }12{ ثُ م َجعَ لنَاه ُ نُ ط َفة فِي َق َرا ر م ِكي ن }13{ ثُ م َخ َل قنَا ال ُّن ط َفة َ َع َل َقة َف َخ َل قنَا ا لعَ َل َقة َ ُم ضغَة َف َخ َل قنَا ا ل ُم ضغَة َ ِع َظا ما َف َك َس ونَا ا ل ِع َظا َم َل ح ما ثُ م أَن َشأنَاه ُ َخ ل قا آ َخ َر َفتَبَا َر َك ّللا ُ أَ ح َس ُن ا ل َخا ِل ِقي َن }14{( Resources BRS Embryology Book. Pathoma Book ( IN DEVELOPMENTAL ANOMALIES PART ). [email protected] 1 OVERVIEW A- Central nervous system (CNS) is formed in week 3 of development, during which time the neural plate develops. The neural plate, consisting of neuroectoderm, becomes the neural tube, which gives rise to the brain and spinal cord. B- Peripheral nervous system (PNS) is derived from three sources: 1. Neural crest cells 2. Neural tube, which gives rise to all preganglionic autonomic nerves (sympathetic and parasympathetic) and all nerves (-motoneurons and -motoneurons) that innervate skeletal muscles 3. Mesoderm, which gives rise to the dura mater and to connective tissue investments of peripheral nerve fibers (endoneurium, perineurium, and epineurium) DEVELOPMENT OF THE NEURAL TUBE Neurulation refers to the formation and closure of the neural tube. BMP-4 (bone morphogenetic protein), noggin (an inductor protein), chordin (an inductor protein), FGF-8 (fibroblast growth factor), and N-CAM (neural cell adhesion molecule) appear to play a role in neurulation. -
Differential Timing and Coordination of Neurogenesis and Astrogenesis
brain sciences Article Differential Timing and Coordination of Neurogenesis and Astrogenesis in Developing Mouse Hippocampal Subregions Allison M. Bond 1, Daniel A. Berg 1, Stephanie Lee 1, Alan S. Garcia-Epelboim 1, Vijay S. Adusumilli 1, Guo-li Ming 1,2,3,4 and Hongjun Song 1,2,3,5,* 1 Department of Neuroscience and Mahoney Institute for Neurosciences, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; [email protected] (A.M.B.); [email protected] (D.A.B.); [email protected] (S.L.); [email protected] (A.S.G.-E.); [email protected] (V.S.A.); [email protected] (G.-l.M.) 2 Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA 3 Institute for Regenerative Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA 4 Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA 5 The Epigenetics Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA * Correspondence: [email protected] Received: 19 October 2020; Accepted: 24 November 2020; Published: 26 November 2020 Abstract: Neocortical development has been extensively studied and therefore is the basis of our understanding of mammalian brain development. One fundamental principle of neocortical development is that neurogenesis and gliogenesis are temporally segregated processes. However, it is unclear how neurogenesis and gliogenesis are coordinated in non-neocortical regions of the cerebral cortex, such as the hippocampus, also known as the archicortex. Here, we show that the timing of neurogenesis and astrogenesis in the Cornu Ammonis (CA) 1 and CA3 regions of mouse hippocampus mirrors that of the neocortex; neurogenesis occurs embryonically, followed by astrogenesis during early postnatal development. -
Anatomically Distinct Patterns of Diffusion MRI Coherence
NeuroImage 79 (2013) 412–422 Contents lists available at SciVerse ScienceDirect NeuroImage journal homepage: www.elsevier.com/locate/ynimg Radial and tangential neuronal migration pathways in the human fetal brain: Anatomically distinct patterns of diffusion MRI coherence James Kolasinski a,c,1, Emi Takahashi a,b,⁎,1, Allison A. Stevens a, Thomas Benner a, Bruce Fischl a, Lilla Zöllei a,b,2, P. Ellen Grant a,b,2 a Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02119, USA b Division of Newborn Medicine, Department of Medicine/Fetal–Neonatal Neuroimaging and Developmental Science Center, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115, USA c Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB), Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK article info abstract Article history: Corticogenesis is underpinned by a complex process of subcortical neuroproliferation, followed by highly orches- Accepted 29 April 2013 trated cellular migration. A greater appreciation of the processes involved in human fetal corticogenesis is vital to Available online 11 May 2013 gaining an understanding of how developmental disturbances originating in gestation could establish a variety of complex neuropathology manifesting in childhood, or even in adult life. Magnetic resonance imaging modalities offer a unique insight into anatomical structure, and increasingly infer information regarding underlying microstructure in the human brain. In this study we applied a combination of high-resolution structural and diffusion-weighted magnetic resonance imaging to a unique cohort of three post-mortem fetal brain specimens, aged between 19 and 22 post-conceptual weeks. -
Astrocyte Calcium Signals at Schaffer Collateral to CA1 Pyramidal Cell Synapses Correlate with the Number of Activated Synapses but Not with Synaptic Strength
HIPPOCAMPUS 00:000–000 (2010) Astrocyte Calcium Signals at Schaffer Collateral to CA1 Pyramidal Cell Synapses Correlate With the Number of Activated Synapses But Not With Synaptic Strength Silke D. Honsek, Corinna Walz, Karl W. Kafitz, and Christine R. Rose* ABSTRACT: Glial cells respond to neuronal activity by transient astrocytes mediate the clearance of glutamate from the increases in their intracellular calcium concentration. At hippocampal extracellular space through high-affinity transporters. Schaffer collateral to CA1 pyramidal cell synapses, such activity-induced This glutamate uptake shapes the time course of syn- astrocyte calcium transients modulate neuronal excitability, synaptic activ- ity, and LTP induction threshold by calcium-dependent release of gliotrans- aptic conductance, moderates the activation of extrasy- mitters. Despite a significant role of astrocyte calcium signaling in plasti- naptic receptors, and limits spillover of glutamate to city of these synapses, little is known about activity-dependent changes of adjacent synapses (Tzingounis and Wadiche, 2007). In astrocyte calcium signaling itself. In this study, we analyzed calcium transi- addition, astrocytes respond to synaptically released stratum radiatum ents in identified astrocytes and NG2-cells located in the glutamate with calcium transients that are mainly in response to different intensities and patterns of Schaffer collateral stimu- lation. To this end, we employed multiphoton calcium imaging with the caused by the activation of metabotropic glutamate low-affinity -
Heterogeneity in Ventricular Zone Neural Precursors Contributes to Neuronal Fate Diversity in the Postnatal Neocortex
7028 • The Journal of Neuroscience, May 19, 2010 • 30(20):7028–7036 Development/Plasticity/Repair Heterogeneity in Ventricular Zone Neural Precursors Contributes to Neuronal Fate Diversity in the Postnatal Neocortex Elizabeth K. Stancik,1 Ivan Navarro-Quiroga,1 Robert Sellke,2 and Tarik F. Haydar1 1Center for Neuroscience Research, Children’s National Medical Center, Washington, DC 20010, and 2University of Maryland School of Medicine, Baltimore, Maryland 21201 The recent discovery of short neural precursors (SNPs) in the murine neocortical ventricular zone (VZ) challenges the widely held view that radial glial cells (RGCs) are the sole occupants of this germinal compartment and suggests that precursor variety is an important factor of brain development. Here, we use in utero electroporation and genetic fate mapping to show that SNPs and RGCs cohabit the VZ but display different cell cycle kinetics and generate phenotypically different progeny. In addition, we find that RGC progeny undergo additional rounds of cell division as intermediate progenitor cells (IPCs), whereas SNP progeny generally produce postmitotic neurons directly from the VZ. By clearly defining SNPs as bona fide VZ residents, separate from both RGCs and IPCs, and uncovering their unique proliferativeandlineageproperties,theseresultsdemonstratehowindividualneuralprecursorgroupsintheembryonicrodentVZcreate diversity in the overlying neocortex. Introduction progenitors properly form the cerebral cortex as well as for elu- The ventricular zone (VZ) of the dorsal telencephalon contains cidating possible mechanisms of species-specific diversity. the progenitor cells that produce all of the various excitatory In addition to the neural precursors in the VZ, a separate class neurons of the mature neocortex. This process occurs during of neuronal progenitors has been described in the overlying sub- prenatal mammalian brain development through a precisely reg- ventricular zone (SVZ). -
Dendritic Size of Pyramidal Neurons Differs Among Mouse Cortical
Cerebral Cortex July 2006;16:990--1001 doi:10.1093/cercor/bhj041 Advance Access publication September 29, 2005 Dendritic Size of Pyramidal Neurons Differs Ruth Benavides-Piccione1,2, Farid Hamzei-Sichani2, Inmaculada Ballesteros-Ya´n˜ez1, Javier DeFelipe1 and Rafael Yuste1,2 among Mouse Cortical Regions 1Instituto Cajal, Madrid, Spain and 2HHMI, Department of Biological Sciences, Columbia University, New York, USA Downloaded from https://academic.oup.com/cercor/article-abstract/16/7/990/425668 by University of Massachusetts Medical School user on 19 February 2019 Neocortical circuits share anatomical and physiological similarities a series of basic circuit diagrams based on anatomical and among different species and cortical areas. Because of this, electrophysiological data (Douglas et al., 1989, 1995; Douglas a ‘canonical’ cortical microcircuit could form the functional unit and Martin, 1991, 1998, 2004). According to their hypothesis, of the neocortex and perform the same basic computation on the common transfer function that the neocortex performs on different types of inputs. However, variations in pyramidal cell inputs could be related to the amplification of the signal structure between different primate cortical areas exist, indicating (Douglas et al., 1989) or a ‘soft’ winner-take-all algorithm that different cortical areas could be built out of different neuronal (Douglas and Martin, 2004). These ideas agree with the re- cell types. In the present study, we have investigated the dendritic current excitation present in cortical tissue which could then architecture of 90 layer II/III pyramidal neurons located in different exert a top-down amplification and selection on thalamic inputs cortical regions along a rostrocaudal axis in the mouse neocortex, (Douglas et al., 1995). -
From Genes to Folds: a Review of Cortical Gyrification Theory
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Springer - Publisher Connector Brain Struct Funct (2015) 220:2475–2483 DOI 10.1007/s00429-014-0961-z REVIEW From genes to folds: a review of cortical gyrification theory Lisa Ronan • Paul C. Fletcher Received: 5 September 2014 / Accepted: 6 December 2014 / Published online: 16 December 2014 Ó The Author(s) 2014. This article is published with open access at Springerlink.com Abstract Cortical gyrification is not a random process. Introduction: key characteristics of gyrification Instead, the folds that develop are synonymous with the functional organization of the cortex, and form patterns A wing would be a most mystifying structure if one that are remarkably consistent across individuals and even did not know that birds flew. One might observe that some species. How this happens is not well understood. it could be extended a considerable distance that it Although many developmental features and evolutionary had a smooth covering of feathers with conspicuous adaptations have been proposed as the primary cause of markings, that it was operated by powerful muscles, gyrencephaly, it is not evident that gyrification is reducible and that strength and lightness were prominent fea- in this way. In recent years, we have greatly increased our tures of its construction. These are important facts, understanding of the multiple factors that influence cortical but by themselves they do not tell us that birds fly. folding, from the action of genes in health and disease to Yet without knowing this, and without understanding evolutionary adaptations that characterize distinctions something of the principles of flight, a more detailed between gyrencephalic and lissencephalic cortices. -
BMP Signaling Suppresses Gemc1 Expression and Ependymal
www.nature.com/scientificreports OPEN BMP signaling suppresses Gemc1 expression and ependymal diferentiation of mouse telencephalic progenitors Hanae Omiya1, Shima Yamaguchi1, Tomoyuki Watanabe1, Takaaki Kuniya1, Yujin Harada1, Daichi Kawaguchi1* & Yukiko Gotoh1,2* The lateral ventricles of the adult mammalian brain are lined by a single layer of multiciliated ependymal cells, which generate a fow of cerebrospinal fuid through directional beating of their cilia as well as regulate neurogenesis through interaction with adult neural stem cells. Ependymal cells are derived from a subset of embryonic neural stem-progenitor cells (NPCs, also known as radial glial cells) that becomes postmitotic during the late embryonic stage of development. Members of the Geminin family of transcriptional regulators including GemC1 and Mcidas play key roles in the diferentiation of ependymal cells, but it remains largely unclear what extracellular signals regulate these factors and ependymal diferentiation during embryonic and early-postnatal development. We now show that the levels of Smad1/5/8 phosphorylation and Id1/4 protein expression—both of which are downstream events of bone morphogenetic protein (BMP) signaling—decline in cells of the ventricular- subventricular zone in the mouse lateral ganglionic eminence in association with ependymal diferentiation. Exposure of postnatal NPC cultures to BMP ligands or to a BMP receptor inhibitor suppressed and promoted the emergence of multiciliated ependymal cells, respectively. Moreover, treatment of embryonic NPC cultures with BMP ligands reduced the expression level of the ependymal marker Foxj1 and suppressed the emergence of ependymal-like cells. Finally, BMP ligands reduced the expression levels of Gemc1 and Mcidas in postnatal NPC cultures, whereas the BMP receptor inhibitor increased them. -
Dendritic Size of Pyramidal Neurons Differs Among Mouse Cortical
Cerebral Cortex July 2006;16:990--1001 doi:10.1093/cercor/bhj041 Advance Access publication September 29, 2005 Dendritic Size of Pyramidal Neurons Differs Ruth Benavides-Piccione1,2, Farid Hamzei-Sichani2, Inmaculada Ballesteros-Ya´n˜ez1, Javier DeFelipe1 and Rafael Yuste1,2 among Mouse Cortical Regions 1Instituto Cajal, Madrid, Spain and 2HHMI, Department of Biological Sciences, Columbia University, New York, USA Neocortical circuits share anatomical and physiological similarities a series of basic circuit diagrams based on anatomical and Downloaded from https://academic.oup.com/cercor/article/16/7/990/425668 by guest on 30 September 2021 among different species and cortical areas. Because of this, electrophysiological data (Douglas et al., 1989, 1995; Douglas a ‘canonical’ cortical microcircuit could form the functional unit and Martin, 1991, 1998, 2004). According to their hypothesis, of the neocortex and perform the same basic computation on the common transfer function that the neocortex performs on different types of inputs. However, variations in pyramidal cell inputs could be related to the amplification of the signal structure between different primate cortical areas exist, indicating (Douglas et al., 1989) or a ‘soft’ winner-take-all algorithm that different cortical areas could be built out of different neuronal (Douglas and Martin, 2004). These ideas agree with the re- cell types. In the present study, we have investigated the dendritic current excitation present in cortical tissue which could then architecture of 90 layer II/III pyramidal neurons located in different exert a top-down amplification and selection on thalamic inputs cortical regions along a rostrocaudal axis in the mouse neocortex, (Douglas et al., 1995). -
Early Dorsomedial Tissue Interactions Regulate Gyrification of Distal
ARTICLE https://doi.org/10.1038/s41467-019-12913-z OPEN Early dorsomedial tissue interactions regulate gyrification of distal neocortex Victor V. Chizhikov1*, Igor Y. Iskusnykh 1, Ekaterina Y. Steshina1, Nikolai Fattakhov 1, Anne G. Lindgren2, Ashwin S. Shetty3, Achira Roy 4, Shubha Tole3 & Kathleen J. Millen4,5* The extent of neocortical gyrification is an important determinant of a species’ cognitive abilities, yet the mechanisms regulating cortical gyrification are poorly understood. We 1234567890():,; uncover long-range regulation of this process originating at the telencephalic dorsal midline, where levels of secreted Bmps are maintained by factors in both the neuroepithelium and the overlying mesenchyme. In the mouse, the combined loss of transcription factors Lmx1a and Lmx1b, selectively expressed in the midline neuroepithelium and the mesenchyme respec- tively, causes dorsal midline Bmp signaling to drop at early neural tube stages. This alters the spatial and temporal Wnt signaling profile of the dorsal midline cortical hem, which in turn causes gyrification of the distal neocortex. Our study uncovers early mesenchymal- neuroepithelial interactions that have long-range effects on neocortical gyrification and shows that lissencephaly in mice is actively maintained via redundant genetic regulation of dorsal midline development and signaling. 1 Department of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, TN 38163, USA. 2 Department of Human Genetics, University of Chicago, Chicago, IL 60637, USA. 3 Department of Biological Sciences, Tata Institute of Fundamental Research, Mumbai, India. 4 Center for Integrative Brain Research, Seattle Children’s Research Institute, Seattle, WA 98101, USA. 5 Department of Pediatrics, University of Washington, Seattle, WA 98101, USA.