Contribution of Apical and Basal Dendrites of L2/3 Pyramidal Neurons to Orientation Encoding in Mouse V1 Jiyoung Park1,4*†, Athanasia Papoutsi3†, Ryan T
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Biophysically Realistic Neuron Models for Simulation of Cortical Stimulation
bioRxiv preprint doi: https://doi.org/10.1101/328534; this version posted August 20, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Biophysically Realistic Neuron Models for Simulation of Cortical Stimulation Authors: Aman S. Aberra1, Angel V. Peterchev1,2,3,4, Warren M. Grill1,3,4,5,* 1 Dept. of Biomedical Engineering, School of Engineering, Duke University, NC 2 Dept. of Psychiatry and Behavioral Sciences, School of Medicine, Duke University, NC 3 Dept. of Electrical and Computer Engineering, School of Engineering, Duke University, NC 4 Dept. of Neurosurgery, School of Medicine, Duke University, NC 5 Dept. of Neurobiology, School of Medicine, Duke University, NC * Corresponding Author: Warren M. Grill Keywords: neuron model, cortex, myelination, simulation, electric field, stimulation, axon bioRxiv preprint doi: https://doi.org/10.1101/328534; this version posted August 20, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 2 1. Abstract Objective. We implemented computational models of human and rat cortical neurons for simulating the neural response to cortical stimulation with electromagnetic fields. Approach. We adapted model neurons from the library of Blue Brain models to reflect biophysical and geometric properties of both adult rat and human cortical neurons and coupled the model neurons to exogenous electric fields (E-fields). The models included 3D reconstructed axonal and dendritic arbors, experimentally-validated electrophysiological behaviors, and multiple, morphological variants within cell types. -
Improved Calcium Sensor Gcamp-X Overcomes the Calcium Channel Perturbations Induced by the Calmodulin in Gcamp
ARTICLE DOI: 10.1038/s41467-018-03719-6 OPEN Improved calcium sensor GCaMP-X overcomes the calcium channel perturbations induced by the calmodulin in GCaMP Yaxiong Yang 1,2,3,4, Nan Liu1,7, Yuanyuan He1, Yuxia Liu1, Lin Ge1, Linzhi Zou5, Sen Song1,4, Wei Xiong4,5 & Xiaodong Liu 1,2,3,4,5,6 2+ 1234567890():,; GCaMP, one popular type of genetically-encoded Ca indicator, has been associated with various side-effects. Here we unveil the intrinsic problem prevailing over different versions and applications, showing that GCaMP containing CaM (calmodulin) interferes with both gating and signaling of L-type calcium channels (CaV1). GCaMP acts as an impaired apoCaM 2+ 2+ and Ca /CaM, both critical to CaV1, which disrupts Ca dynamics and gene expression. We then design and implement GCaMP-X, by incorporating an extra apoCaM-binding motif, effectively protecting CaV1-dependent excitation–transcription coupling from perturbations. GCaMP-X resolves the problems of detrimental nuclear accumulation, acute and chronic Ca2+ dysregulation, and aberrant transcription signaling and cell morphogenesis, while still demonstrating excellent Ca2+-sensing characteristics partly inherited from GCaMP. In summary, CaM/CaV1 gating and signaling mechanisms are elucidated for GCaMP side- effects, while allowing the development of GCaMP-X to appropriately monitor cytosolic, submembrane or nuclear Ca2+, which is also expected to guide the future design of CaM- based molecular tools. 1 Department of Biomedical Engineering, School of Medicine, X-Lab for Transmembrane Signaling Research, Tsinghua University, Beijing 100084, China. 2 School of Biological Science and Medical Engineering, Beihang University, Beijing 100083, China. 3 Beijing Advanced Innovation Center for Biomedical Engineering, Beihang University, Beijing 102402, China. -
Neuronal Organization of Olfactory Bulb Circuits
REVIEW ARTICLE published: 03 September 2014 doi: 10.3389/fncir.2014.00098 Neuronal organization of olfactory bulb circuits Shin Nagayama 1*, Ryota Homma1 and Fumiaki Imamura 2 1 Department of Neurobiology and Anatomy, The University of Texas Medical School at Houston, Houston, TX, USA 2 Department of Pharmacology, Pennsylvania State University College of Medicine, Hershey, PA, USA Edited by: Olfactory sensory neurons extend their axons solely to the olfactory bulb, which is Benjamin R. Arenkiel, Baylor College dedicated to odor information processing.The olfactory bulb is divided into multiple layers, of Medicine, USA with different types of neurons found in each of the layers. Therefore, neurons in the Reviewed by: olfactory bulb have conventionally been categorized based on the layers in which their cell Kazushige Touhara, University of Tokyo, Japan bodies are found; namely, juxtaglomerular cells in the glomerular layer, tufted cells in the Veronica Egger, external plexiform layer, mitral cells in the mitral cell layer, and granule cells in the granule Ludwig-Maximilians-Universität, cell layer. More recently, numerous studies have revealed the heterogeneous nature of each Germany Kathleen Quast, Baylor College of of these cell types, allowing them to be further divided into subclasses based on differences Medicine, USA in morphological, molecular, and electrophysiological properties. In addition, technical *Correspondence: developments and advances have resulted in an increasing number of studies regarding Shin Nagayama, Department of cell types other than the conventionally categorized ones described above, including short- Neurobiology and Anatomy, The axon cells and adult-generated interneurons. Thus, the expanding diversity of cells in the University of Texas Medical School at Houston, 6431 Fannin Street, olfactory bulb is now being acknowledged. -
Action Potentials in Basal and Oblique Dendrites of Rat Neocortical Pyramidal Neurons Srdjan D
Physiology in Press; published online on May 9, 2003 as 10.1113/jphysiol.2002.033746 J Physiol (2003), xxx.x, pp. 000–000 DOI: 10.1113/jphysiol.2002.033746 © The Physiological Society 2003 www.jphysiol.org Action potentials in basal and oblique dendrites of rat neocortical pyramidal neurons Srdjan D. Antic Department of Cellular and Molecular Physiology, and Department of Neurobiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA Basal and oblique dendrites comprise ~2/3 of the total excitable membrane in the mammalian cerebral cortex, yet they have never been probed with glass electrodes, and therefore their electrical properties and overall impact on synaptic processing are unknown. In the present study, fast multi- site voltage-sensitive dye imaging combined with somatic recording was used to provide a detailed description of the membrane potential transients in basal and oblique dendrites of pyramidal neurons during single and trains of action potentials (APs). The optical method allowed simultaneous measurements from several dendrites in the visual field up to 200 mm from the soma, thus providing a unique report on how an AP invades the entire dendritic tree. In contrast to apical dendrites, basal and oblique branches: (1) impose very little amplitude and time course modulation on backpropagating APs; (2) are strongly invaded by the somatic spike even when somatic firing rates reach 40 Hz (activity-independent backpropagation); and (3) do not exhibit signs of a ‘calcium shoulder’ on the falling phase of the AP. A compartmental model incorporating AP peak latencies and half-widths obtained from the apical, oblique and basal dendrites indicates that the specific intracellular resistance (Ri) is less than 100 V cm. -
Transient Hypoxemia Chronically Disrupts Maturation of Preterm Fetal Ovine Subplate Neuron Arborization and Activity
11912 • The Journal of Neuroscience, December 6, 2017 • 37(49):11912–11929 Development/Plasticity/Repair Transient Hypoxemia Chronically Disrupts Maturation of Preterm Fetal Ovine Subplate Neuron Arborization and Activity XEvelyn McClendon,1 Daniel C. Shaver,1 Kiera Degener-O’Brien,1 Xi Gong,1 Thuan Nguyen,2 Anna Hoerder-Suabedissen,3 Zolta´n Molna´r,3 Claudia Mohr,4 XBen D. Richardson,4 David J. Rossi,4 and Stephen A. Back1,5 1Department of Pediatrics and 2Public Health and Preventive Medicine, Oregon Health & Science University, Portland, Oregon 97239, 3Department of Physiology, Anatomy, and Genetics, University of Oxford, Oxford, United Kingdom OX1 3QX, 4Department of Integrative Physiology and Neuroscience, College of Veterinary Medicine, Washington State University, Pullman, Washington 99164, and 5Department of Neurology, Oregon Health & Science University, Portland, Oregon 97239 Preterm infants are at risk for a broad spectrum of neurobehavioral disabilities associated with diffuse disturbances in cortical growth and development. During brain development, subplate neurons (SPNs) are a largely transient population that serves a critical role to establish functional cortical circuits. By dynamically integrating into developing cortical circuits, they assist in consolidation of intra- cortical and extracortical circuits. Although SPNs reside in close proximity to cerebral white matter, which is particularly vulnerable to oxidative stress, the susceptibility of SPNs remains controversial. We determined SPN responses to two common insults to the preterm brain: hypoxia-ischemia and hypoxia. We used a preterm fetal sheep model using both sexes that reproduces the spectrum of human cerebral injury and abnormal cortical growth. Unlike oligodendrocyte progenitors, SPNs displayed pronounced resistance to early or delayed cell death from hypoxia or hypoxia-ischemia. -
Autism Spectrum Disorder Susceptibility Gene TAOK2 Affects
ART ic LE s Autism spectrum disorder susceptibility gene TAOK2 affects basal dendrite formation in the neocortex Froylan Calderon de Anda1,2, Ana Lucia Rosario1,2, Omer Durak1–3, Tracy Tran2,4,5, Johannes Gräff1,2, Konstantinos Meletis1–3,5, Damien Rei1,2, Takahiro Soda1,2, Ram Madabhushi1,2, David D Ginty2,4, Alex L Kolodkin2,4 & Li-Huei Tsai1–3 How neurons develop their morphology is an important question in neurobiology. Here we describe a new pathway that specifically affects the formation of basal dendrites and axonal projections in cortical pyramidal neurons. We report that thousand-and-one- amino acid 2 kinase (TAOK2), also known as TAO2, is essential for dendrite morphogenesis. TAOK2 downregulation impairs basal dendrite formation in vivo without affecting apical dendrites. Moreover, TAOK2 interacts with Neuropilin 1 (Nrp1), a receptor protein that binds the secreted guidance cue Semaphorin 3A (Sema3A). TAOK2 overexpression restores dendrite formation in cultured cortical neurons from Nrp1Sema− mice, which express Nrp1 receptors incapable of binding Sema3A. TAOK2 overexpression also ameliorates the basal dendrite impairment resulting from Nrp1 downregulation in vivo. Finally, Sema3A and TAOK2 modulate the formation of basal dendrites through the activation of the c-Jun N-terminal kinase (JNK). These results delineate a pathway whereby Sema3A and Nrp1 transduce signals through TAOK2 and JNK to regulate basal dendrite development in cortical neurons. Pyramidal neurons are abundant in brain regions associated with through the activation of JNK11. TAOK2 is subjected to alternative complex cognitive functions, including the cortex, hippocampus and splicing to produce the TAOK2α (140 kDa) and TAOK2β (120 kDa) amygdala1. -
GPCR-Based Dopamine Sensors—A Detailed Guide to Inform Sensor Choice for in Vivo Imaging
International Journal of Molecular Sciences Review GPCR-Based Dopamine Sensors—A Detailed Guide to Inform Sensor Choice for In Vivo Imaging 1,2, 3,4, 4,5, Marie A. Labouesse y, Reto B. Cola y and Tommaso Patriarchi * 1 Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA; [email protected] 2 Division of Molecular Therapeutics, New York State Psychiatric Institute, New York, NY 10032, USA 3 Anatomy and Program in Neuroscience, University of Fribourg, 1700 Fribourg, Switzerland; [email protected] 4 Institute of Pharmacology and Toxicology, University of Zurich, 8057 Zurich, Switzerland 5 Neuroscience Center Zurich, University and ETH Zurich, 8057 Zurich, Switzerland * Correspondence: [email protected]; Tel.: +41-044-635-59-21 These authors share equal co-first contribution. y Received: 10 September 2020; Accepted: 26 September 2020; Published: 28 October 2020 Abstract: Understanding how dopamine (DA) encodes behavior depends on technologies that can reliably monitor DA release in freely-behaving animals. Recently, red and green genetically encoded sensors for DA (dLight, GRAB-DA) were developed and now provide the ability to track release dynamics at a subsecond resolution, with submicromolar affinity and high molecular specificity. Combined with rapid developments in in vivo imaging, these sensors have the potential to transform the field of DA sensing and DA-based drug discovery. When implementing these tools in the laboratory, it is important to consider there is not a ‘one-size-fits-all’ sensor. Sensor properties, most importantly their affinity and dynamic range, must be carefully chosen to match local DA levels. -
Down-Regulation of Dendritic Spine and Glutamic Acid Decarboxylase 67 Expressions in the Reelin Haploinsufficient Heterozygous Reeler Mouse
Down-regulation of dendritic spine and glutamic acid decarboxylase 67 expressions in the reelin haploinsufficient heterozygous reeler mouse Wen Sheng Liu*, Christine Pesold*, Miguel A. Rodriguez*, Giovanni Carboni*, James Auta*, Pascal Lacor*, John Larson*, Brian G. Condie†, Alessandro Guidotti*, and Erminio Costa*‡ *Psychiatric Institute, Department of Psychiatry, College of Medicine, University of Illinois, Chicago, IL 60612; and †Institute of Molecular Medicine and Genetics, Departments of Medicine and Cellular Biology and Anatomy, Medical College of Georgia, Augusta, GA 30912 Contributed by Erminio Costa, December 22, 2000 Heterozygous reeler mice (HRM) haploinsufficient for reelin ex- heterozygote reeler mice (HRM) and in heterozygote GAD67 Ϸ press 50% of the brain reelin content of wild-type mice, but are knockout mice (HG67M) and compared them to their respective phenotypically different from both wild-type mice and homozy- wild-type background mice (WTM). In the present study, we gous reeler mice. They exhibit, (i) a down-regulation of glutamic have also quantified the number of neurons immunopositive for acid decarboxylase 67 (GAD67)-positive neurons in some but not reelin in the motor area of the frontoparietal cortex (FPC) of every cortical layer of frontoparietal cortex (FPC), (ii) an increase of HRM, as well as the total number of neurons immunopositive for neuronal packing density and a decrease of cortical thickness NeuN and the number of glial cells stained by Nissl (13) because of neuropil hypoplasia, (iii) a decrease of dendritic spine expressed in each of the six layers of this cortical area. In WTM, expression density on basal and apical dendritic branches of motor HRM, and HG67M, we have also quantified the laminar expres- FPC layer III pyramidal neurons, and (iv) a similar decrease in sion of GAD67-immunopositive neurons and the dendritic spine dendritic spines expressed on the basal dendrite branches of CA1 density expressed by pyramidal neurons of layer III FPC and of pyramidal neurons of the hippocampus. -
Contribution of Apical and Basal Dendrites to Orientation Encoding in Mouse V1 L2/3 Pyramidal Neurons
ARTICLE https://doi.org/10.1038/s41467-019-13029-0 OPEN Contribution of apical and basal dendrites to orientation encoding in mouse V1 L2/3 pyramidal neurons Jiyoung Park1,2,7*, Athanasia Papoutsi3,7, Ryan T. Ash1,4,5, Miguel A. Marin4,6, Panayiota Poirazi 3,8*& Stelios M. Smirnakis1,8* 1234567890():,; Pyramidal neurons integrate synaptic inputs from basal and apical dendrites to generate stimulus-specific responses. It has been proposed that feed-forward inputs to basal dendrites drive a neuron’s stimulus preference, while feedback inputs to apical dendrites sharpen selectivity. However, how a neuron’s dendritic domains relate to its functional selectivity has not been demonstrated experimentally. We performed 2-photon dendritic micro-dissection on layer-2/3 pyramidal neurons in mouse primary visual cortex. We found that removing the apical dendritic tuft did not alter orientation-tuning. Furthermore, orientation-tuning curves were remarkably robust to the removal of basal dendrites: ablation of 2 basal dendrites was needed to cause a small shift in orientation preference, without significantly altering tuning width. Computational modeling corroborated our results and put limits on how orientation preferences among basal dendrites differ in order to reproduce the post-ablation data. In conclusion, neuronal orientation-tuning appears remarkably robust to loss of dendritic input. 1 Brigham and Women’s Hospital and Jamaica Plain VA Hospital, Harvard Medical School, Boston, MA, USA. 2 Program in Structural and Computational Biology and Molecular Biophysics, Baylor College of Medicine, Houston, TX, USA. 3 Institute of Molecular Biology and Biotechnology (IMBB), Foundation of Research and Technology Hellas (FORTH), Vassilika Vouton, HeraklionCrete, Greece. -
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). -
Sonic Hedgehog Signaling in Astrocytes Mediates Cell Type
RESEARCH ARTICLE Sonic hedgehog signaling in astrocytes mediates cell type-specific synaptic organization Steven A Hill1†, Andrew S Blaeser1†, Austin A Coley2, Yajun Xie3, Katherine A Shepard1, Corey C Harwell3, Wen-Jun Gao2, A Denise R Garcia1,2* 1Department of Biology, Drexel University, Philadelphia, United States; 2Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, United States; 3Department of Neurobiology, Harvard Medical School, Boston, United States Abstract Astrocytes have emerged as integral partners with neurons in regulating synapse formation and function, but the mechanisms that mediate these interactions are not well understood. Here, we show that Sonic hedgehog (Shh) signaling in mature astrocytes is required for establishing structural organization and remodeling of cortical synapses in a cell type-specific manner. In the postnatal cortex, Shh signaling is active in a subpopulation of mature astrocytes localized primarily in deep cortical layers. Selective disruption of Shh signaling in astrocytes produces a dramatic increase in synapse number specifically on layer V apical dendrites that emerges during adolescence and persists into adulthood. Dynamic turnover of dendritic spines is impaired in mutant mice and is accompanied by an increase in neuronal excitability and a reduction of the glial-specific, inward-rectifying K+ channel Kir4.1. These data identify a critical role for Shh signaling in astrocyte-mediated modulation of neuronal activity required for sculpting synapses. *For correspondence: DOI: https://doi.org/10.7554/eLife.45545.001 [email protected] †These authors contributed equally to this work Introduction Competing interests: The The organization of synapses into the appropriate number and distribution occurs through a process authors declare that no of robust synapse addition followed by a period of refinement during which excess synapses are competing interests exist. -
Live Imaging of Calcium Dynamics During Axon Degeneration Reveals Two Functionally Distinct Phases of Calcium Influx
15026 • The Journal of Neuroscience, November 11, 2015 • 35(45):15026–15038 Development/Plasticity/Repair Live Imaging of Calcium Dynamics during Axon Degeneration Reveals Two Functionally Distinct Phases of Calcium Influx X Mauricio Enrique Vargas,1,2 XYuya Yamagishi,3 Marc Tessier-Lavigne,3 and Alvaro Sagasti1 1Department of Molecular, Cell, and Developmental Biology, University of California, Los Angeles, California 90095, 2Jules Stein Eye Institute and Department of Ophthalmology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, and 3Laboratory of Brain Development and Repair, The Rockefeller University, New York, New York 10065 Calcium is a key regulator of axon degeneration caused by trauma and disease, but its specific spatial and temporal dynamics in injured axons remain unclear. To clarify the function of calcium in axon degeneration, we observed calcium dynamics in single injured neurons in live zebrafish larvae and tested the temporal requirement for calcium in zebrafish neurons and cultured mouse DRG neurons. Using laser axotomy to induce Wallerian degeneration (WD) in zebrafish peripheral sensory axons, we monitored calcium dynamics from injury to fragmentation, revealing two stereotyped phases of axonal calcium influx. First, axotomy triggered a transient local calcium wave originating at the injury site. This initial calcium wave only disrupted mitochondria near the injury site and was not altered by expression of the protective WD slow (WldS) protein. Inducing multiple waves with additional axotomies did not change the kinetics of degeneration. In contrast, a second phase of calcium influx occurring minutes before fragmentation spread as a wave throughout the axon, entered mitochondria, and was abolished by WldS expression.