Differential Timing and Coordination of Neurogenesis and Astrogenesis
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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. -
Neuregulin 1–Erbb2 Signaling Is Required for the Establishment of Radial Glia and Their Transformation Into Astrocytes in Cerebral Cortex
Neuregulin 1–erbB2 signaling is required for the establishment of radial glia and their transformation into astrocytes in cerebral cortex Ralf S. Schmid*, Barbara McGrath*, Bridget E. Berechid†, Becky Boyles*, Mark Marchionni‡, Nenad Sˇ estan†, and Eva S. Anton*§ *University of North Carolina Neuroscience Center and Department of Cell and Molecular Physiology, University of North Carolina School of Medicine, Chapel Hill, NC 27599; †Department of Neurobiology, Yale University School of Medicine, New Haven, CT 06510; and ‡CeNes Pharamceuticals, Inc., Norwood, MA 02062 Communicated by Pasko Rakic, Yale University School of Medicine, New Haven, CT, January 27, 2003 (received for review December 12, 2002) Radial glial cells and astrocytes function to support the construction mine whether NRG-1-mediated signaling is involved in radial and maintenance, respectively, of the cerebral cortex. However, the glial cell development and differentiation in the cerebral cortex. mechanisms that determine how radial glial cells are established, We show that NRG-1 signaling, involving erbB2, may act in maintained, and transformed into astrocytes in the cerebral cortex are concert with Notch signaling to exert a critical influence in the not well understood. Here, we show that neuregulin-1 (NRG-1) exerts establishment, maintenance, and appropriate transformation of a critical role in the establishment of radial glial cells. Radial glial cell radial glial cells in cerebral cortex. generation is significantly impaired in NRG mutants, and this defect can be rescued by exogenous NRG-1. Down-regulation of expression Materials and Methods and activity of erbB2, a member of the NRG-1 receptor complex, leads Clonal Analysis to Study NRG’s Role in the Initial Establishment of to the transformation of radial glial cells into astrocytes. -
Regulation of Adult Neurogenesis in Mammalian Brain
International Journal of Molecular Sciences Review Regulation of Adult Neurogenesis in Mammalian Brain 1,2, 3, 3,4 Maria Victoria Niklison-Chirou y, Massimiliano Agostini y, Ivano Amelio and Gerry Melino 3,* 1 Centre for Therapeutic Innovation (CTI-Bath), Department of Pharmacy & Pharmacology, University of Bath, Bath BA2 7AY, UK; [email protected] 2 Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK 3 Department of Experimental Medicine, TOR, University of Rome “Tor Vergata”, 00133 Rome, Italy; [email protected] (M.A.); [email protected] (I.A.) 4 School of Life Sciences, University of Nottingham, Nottingham NG7 2HU, UK * Correspondence: [email protected] These authors contributed equally to this work. y Received: 18 May 2020; Accepted: 7 July 2020; Published: 9 July 2020 Abstract: Adult neurogenesis is a multistage process by which neurons are generated and integrated into existing neuronal circuits. In the adult brain, neurogenesis is mainly localized in two specialized niches, the subgranular zone (SGZ) of the dentate gyrus and the subventricular zone (SVZ) adjacent to the lateral ventricles. Neurogenesis plays a fundamental role in postnatal brain, where it is required for neuronal plasticity. Moreover, perturbation of adult neurogenesis contributes to several human diseases, including cognitive impairment and neurodegenerative diseases. The interplay between extrinsic and intrinsic factors is fundamental in regulating neurogenesis. Over the past decades, several studies on intrinsic pathways, including transcription factors, have highlighted their fundamental role in regulating every stage of neurogenesis. However, it is likely that transcriptional regulation is part of a more sophisticated regulatory network, which includes epigenetic modifications, non-coding RNAs and metabolic pathways. -
Early Neuronal and Glial Fate Restriction of Embryonic Neural Stem Cells
The Journal of Neuroscience, March 5, 2008 • 28(10):2551–2562 • 2551 Development/Plasticity/Repair Early Neuronal and Glial Fate Restriction of Embryonic Neural Stem Cells Delphine Delaunay,1,2 Katharina Heydon,1,2 Ana Cumano,3 Markus H. Schwab,4 Jean-Le´on Thomas,1,2 Ueli Suter,5 Klaus-Armin Nave,4 Bernard Zalc,1,2 and Nathalie Spassky1,2 1Inserm, Unite´ 711, 75013 Paris, France, 2Institut Fe´de´ratif de Recherche 70, Faculte´deMe´decine, Universite´ Pierre et Marie Curie, 75013 Paris, France, 3Inserm, Unite´ 668, Institut Pasteur, 75724 Paris Cedex 15, France, 4Max-Planck-Institute of Experimental Medicine, D-37075 Goettingen, Germany, and 5Institute of Cell Biology, Swiss Federal Institute of Technology (ETH), ETH Ho¨nggerberg, CH-8093 Zu¨rich, Switzerland The question of how neurons and glial cells are generated during the development of the CNS has over time led to two alternative models: either neuroepithelial cells are capable of giving rise to neurons first and to glial cells at a later stage (switching model), or they are intrinsically committed to generate one or the other (segregating model). Using the developing diencephalon as a model and by selecting a subpopulation of ventricular cells, we analyzed both in vitro, using clonal analysis, and in vivo, using inducible Cre/loxP fate mapping, the fate of neuroepithelial and radial glial cells generated at different time points during embryonic development. We found that, during neurogenic periods [embryonic day 9.5 (E9.5) to 12.5], proteolipid protein ( plp)-expressing cells were lineage-restricted neuronal precursors, but later in embryogenesis, during gliogenic periods (E13.5 to early postnatal), plp-expressing cells were lineage-restricted glial precursors. -
Notch-Signaling in Retinal Regeneration and Müller Glial Plasticity
Notch-Signaling in Retinal Regeneration and Müller glial Plasticity DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Kanika Ghai, MS Neuroscience Graduate Studies Program The Ohio State University 2009 Dissertation Committee: Dr. Andy J Fischer, Advisor Dr. Heithem El-Hodiri Dr. Susan Cole Dr. Paul Henion Copyright by Kanika Ghai 2009 ABSTRACT Eye diseases such as blindness, age-related macular degeneration (AMD), diabetic retinopathy and glaucoma are highly prevalent in the developed world, especially in a rapidly aging population. These sight-threatening diseases all involve the progressive loss of cells from the retina, the light-sensing neural tissue that lines the back of the eye. Thus, developing strategies to replace dying retinal cells or prolonging neuronal survival is essential to preserving sight. In this regard, cell-based therapies hold great potential as a treatment for retinal diseases. One strategy is to stimulate cells within the retina to produce new neurons. This dissertation elucidates the properties of the primary support cell in the chicken retina, known as the Müller glia, which have recently been shown to possess stem-cell like properties, with the potential to form new neurons in damaged retinas. However, the mechanisms that govern this stem-cell like ability are less well understood. In order to better understand these properties, we analyze the role of one of the key developmental processes, i.e., the Notch-Signaling Pathway in regulating proliferative, neuroprotective and regenerative properties of Müller glia and bestow them with this plasticity. -
Postnatal Neurogenesis and Gliogenesis in the Olfactory Bulb from NG2-Expressing Progenitors of the Subventricular Zone
10530 • The Journal of Neuroscience, November 17, 2004 • 24(46):10530–10541 Development/Plasticity/Repair Postnatal Neurogenesis and Gliogenesis in the Olfactory Bulb from NG2-Expressing Progenitors of the Subventricular Zone Adan Aguirre and Vittorio Gallo Center for Neuroscience Research, Children’s Research Institute, Children’s National Medical Center, Washington, DC 20010 We used a 2Ј,3Ј-cyclic nucleotide 3Ј-phosphodiesterase (CNP)–enhanced green fluorescent protein (EGFP) transgenic mouse to study postnatal subventricular zone (SVZ) progenitor fate, with a focus on the olfactory bulb (OB). The postnatal OB of the CNP–EGFP mouse contained EGFP ϩ interneurons and oligodendrocytes. In the anterior SVZ, the majority of EGFP ϩ progenitors were NG2 ϩ. These NG2 ϩ/EGFP ϩ progenitors expressed the OB interneuron marker Er81, the neuroblast markers doublecortin (DC) and Distalless-related homeobox (DLX), or the oligodendrocyte progenitor marker Nkx2.2. In the rostral migratory stream (RMS), EGFP ϩ cells displayed a migrating phenotype. A fraction of these cells were either NG2 Ϫ/Er81 ϩ/DC ϩ/DLX ϩ or NG2 ϩ/Nkx2.2 ϩ. DiI (1,1Ј-dioctadecyl-3,3,3Ј,3Ј- tetramethylindocarbocyanine perchlorate) injection into the lateral ventricle (LV) of early postnatal mice demonstrated that NG2ϩ/ EGFP ϩ progenitors migrate from the SVZ through the RMS into the OB. Moreover, fluorescence-activated cell-sorting-purified NG2ϩ/ CNP–EGFP ϩ or NG2 ϩ/-actin–enhanced yellow fluorescent protein-positive (EYFP ϩ) progenitors transplanted into the early postnatal LV displayed extensive rostral and caudal migration. EYFP ϩ or EGFP ϩ graft-derived cells within the RMS were DLX ϩ/Er81 ϩ or Nkx2.2 ϩ, migrated to the OB, and differentiated to interneurons and oligodendrocytes. -
Microglia Enhance Neurogenesis and Oligodendrogenesis in the Early Postnatal Subventricular Zone
The Journal of Neuroscience, February 5, 2014 • 34(6):2231–2243 • 2231 Development/Plasticity/Repair Microglia Enhance Neurogenesis and Oligodendrogenesis in the Early Postnatal Subventricular Zone Yukari Shigemoto-Mogami,1 Kazue Hoshikawa,1 James E. Goldman,2 Yuko Sekino,1 and Kaoru Sato1 1Laboratory of Neuropharmacology, Division of Pharmacology, National Institute of Health Sciences, Tokyo 158-8501, Japan, and 2Department of Pathology and Cell Biology, Columbia University College of Physicians and Surgeons, New York, New York 10032 Although microglia have long been considered as brain resident immune cells, increasing evidence suggests that they also have physio- logical roles in the development of the normal CNS. In this study, we found large numbers of activated microglia in the forebrain subventricular zone (SVZ) of the rat from P1 to P10. Pharmacological suppression of the activation, which produces a decrease in levels of a number of proinflammatory cytokines (i.e., IL-1, IL-6, TNF-␣, and IFN-␥) significantly inhibited neurogenesis and oligodendro- genesis in the SVZ. In vitro neurosphere assays reproduced the enhancement of neurogenesis and oligodendrogenesis by activated microglia and showed that the cytokines revealed the effects complementarily. These results suggest that activated microglia accumulate in the early postnatal SVZ and that they enhance neurogenesis and oligodendrogenesis via released cytokines. Key words: cytokine; microglia; neurogenesis; neurosphere; oligodendrogenesis; subventricular zone Introduction SVZ -
Transcription Factor Lhx2 Is Necessary and Sufficient to Suppress
Transcription factor Lhx2 is necessary and sufficient PNAS PLUS to suppress astrogliogenesis and promote neurogenesis in the developing hippocampus Lakshmi Subramaniana,1, Anindita Sarkara,1, Ashwin S. Shettya, Bhavana Muralidharana, Hari Padmanabhana, Michael Piperb, Edwin S. Monukic, Ingolf Bachd, Richard M. Gronostajskie,f, Linda J. Richardsb, and Shubha Tolea,2 aDepartment of Biological Sciences, Tata Institute of Fundamental Research, Mumbai 400005, India; bQueensland Brain Institute and School of Biomedical Sciences, University of Queensland, Brisbane, Queensland 4072, Australia; cDepartment of Pathology and Laboratory Medicine, School of Medicine, University of California, Irvine, CA 92697; dPrograms in Gene Function and Expression and Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605; eDepartment of Biochemistry, State University of New York, Buffalo, NY 14203; and fDevelopmental Genomics Group, New York State Center of Excellence in Bioinformatics and Life Sciences, Buffalo, NY 14203 AUTHOR SUMMARY During the development of the verte- memory. We used two approaches to brate CNS, progenitor cells generate disrupt Lhx2 function in progenitors at neurons, the primary players in circuits, the peak of hippocampal neurogenesis, and glia, the support cells. A character- embryonic gestation day (E) 15. Condi- istic feature of this process, common to tional KO mice were used, in which the all vertebrate species, is that the pro- gene encoding Lhx2 protein was dis- duction of neurons precedes that of glial rupted by the introduction of an enzyme cells (1). The transition from neuro- called “Cre recombinase,” which can cut genesis to gliogenesis determines the and paste DNA (2). The second ap- number of neurons vs. support cells that proach used a “dominant-negative” con- NEUROSCIENCE are produced in a given structure. -
NEUROGENESIS in the ADULT BRAIN: New Strategies for Central Nervous System Diseases
7 Jan 2004 14:25 AR AR204-PA44-17.tex AR204-PA44-17.sgm LaTeX2e(2002/01/18) P1: GCE 10.1146/annurev.pharmtox.44.101802.121631 Annu. Rev. Pharmacol. Toxicol. 2004. 44:399–421 doi: 10.1146/annurev.pharmtox.44.101802.121631 Copyright c 2004 by Annual Reviews. All rights reserved First published online as a Review in Advance on August 28, 2003 NEUROGENESIS IN THE ADULT BRAIN: New Strategies for Central Nervous System Diseases ,1 ,2 D. Chichung Lie, Hongjun Song, Sophia A. Colamarino,1 Guo-li Ming,2 and Fred H. Gage1 1Laboratory of Genetics, The Salk Institute, La Jolla, California 92037; email: [email protected], [email protected], [email protected] 2Institute for Cell Engineering, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287; email: [email protected], [email protected] Key Words adult neural stem cells, regeneration, recruitment, cell replacement, therapy ■ Abstract New cells are continuously generated from immature proliferating cells throughout adulthood in many organs, thereby contributing to the integrity of the tissue under physiological conditions and to repair following injury. In contrast, repair mechanisms in the adult central nervous system (CNS) have long been thought to be very limited. However, recent findings have clearly demonstrated that in restricted areas of the mammalian brain, new functional neurons are constantly generated from neural stem cells throughout life. Moreover, stem cells with the potential to give rise to new neurons reside in many different regions of the adult CNS. These findings raise the possibility that endogenous neural stem cells can be mobilized to replace dying neurons in neurodegenerative diseases. -
Concerted Control of Gliogenesis by Inr/TOR and FGF Signalling in the Drosophila Post-Embryonic Brain Amélie Avet-Rochex1, Aamna K
RESEARCH ARTICLE 2763 Development 139, 2763-2772 (2012) doi:10.1242/dev.074179 © 2012. Published by The Company of Biologists Ltd Concerted control of gliogenesis by InR/TOR and FGF signalling in the Drosophila post-embryonic brain Amélie Avet-Rochex1, Aamna K. Kaul1, Ariana P. Gatt1, Helen McNeill2 and Joseph M. Bateman1,* SUMMARY Glial cells are essential for the development and function of the nervous system. In the mammalian brain, vast numbers of glia of several different functional types are generated during late embryonic and early foetal development. However, the molecular cues that instruct gliogenesis and determine glial cell type are poorly understood. During post-embryonic development, the number of glia in the Drosophila larval brain increases dramatically, potentially providing a powerful model for understanding gliogenesis. Using glial-specific clonal analysis we find that perineural glia and cortex glia proliferate extensively through symmetric cell division in the post-embryonic brain. Using pan-glial inhibition and loss-of-function clonal analysis we find that Insulin-like receptor (InR)/Target of rapamycin (TOR) signalling is required for the proliferation of perineural glia. Fibroblast growth factor (FGF) signalling is also required for perineural glia proliferation and acts synergistically with the InR/TOR pathway. Cortex glia require InR in part, but not downstream components of the TOR pathway, for proliferation. Moreover, cortex glia absolutely require FGF signalling, such that inhibition of the FGF pathway almost completely blocks the generation of cortex glia. Neuronal expression of the FGF receptor ligand Pyramus is also required for the generation of cortex glia, suggesting a mechanism whereby neuronal FGF expression coordinates neurogenesis and cortex gliogenesis. -
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 -
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).