NEURAL CONNECTIONS: Some You Use, Some You Lose
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Crayfish Escape Behavior and Central Synapses
Crayfish Escape Behavior and Central Synapses. III. Electrical Junctions and Dendrite Spikes in Fast Flexor Motoneurons ROBERT S. ZUCKER Department of Biological Sciences and Program in the Neurological Sciences, Stanford University, Stanford, California 94305 THE LATERAL giant fiber is the decision fiber and fast flexor motoneurons are located in for a behavioral response in crayfish in- the dorsal neuropil of each abdominal gan- volving rapid tail flexion in response to glion. Dye injections and anatomical recon- abdominal tactile stimulation (27). Each structions of ‘identified motoneurons reveal lateral giant impulse is followed by a rapid that only those motoneurons which have tail flexion or tail flip, and when the giant dentritic branches in contact with a giant fiber does not fire in response to such stim- fiber are activated by that giant fiber (12, uli, the movement does not occur. 21). All of tl ie fast flexor motoneurons are The afferent limb of the reflex exciting excited by the ipsilateral giant; all but F4, the lateral giant has been described (28), F5 and F7 are also excited by the contra- and the habituation of the behavior has latkral giant (21 a). been explained in terms of the properties The excitation of these motoneurons, of this part of the neural circuit (29). seen as depolarizing potentials in their The properties of the neuromuscular somata, does not always reach threshold for junctions between the fast flexor motoneu- generating a spike which propagates out the rons and the phasic flexor muscles have also axon to the periphery (14). Indeed, only t,he been described (13). -
Long-Term Adult Human Brain Slice Cultures As a Model System to Study
TOOLS AND RESOURCES Long-term adult human brain slice cultures as a model system to study human CNS circuitry and disease Niklas Schwarz1, Betu¨ l Uysal1, Marc Welzer2,3, Jacqueline C Bahr1, Nikolas Layer1, Heidi Lo¨ ffler1, Kornelijus Stanaitis1, Harshad PA1, Yvonne G Weber1,4, Ulrike BS Hedrich1, Ju¨ rgen B Honegger4, Angelos Skodras2,3, Albert J Becker5, Thomas V Wuttke1,4†*, Henner Koch1†* 1Department of Neurology and Epileptology, Hertie-Institute for Clinical Brain Research, University of Tu¨ bingen, Tu¨ bingen, Germany; 2Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, University of Tu¨ bingen, Tu¨ bingen, Germany; 3German Center for Neurodegenerative Diseases (DZNE), Tu¨ bingen, Germany; 4Department of Neurosurgery, University of Tu¨ bingen, Tu¨ bingen, Germany; 5Department of Neuropathology, Section for Translational Epilepsy Research, University Bonn Medical Center, Bonn, Germany Abstract Most of our knowledge on human CNS circuitry and related disorders originates from model organisms. How well such data translate to the human CNS remains largely to be determined. Human brain slice cultures derived from neurosurgical resections may offer novel avenues to approach this translational gap. We now demonstrate robust preservation of the complex neuronal cytoarchitecture and electrophysiological properties of human pyramidal neurons *For correspondence: in long-term brain slice cultures. Further experiments delineate the optimal conditions for efficient [email protected] viral transduction of cultures, enabling ‘high throughput’ fluorescence-mediated 3D reconstruction tuebingen.de (TVW); of genetically targeted neurons at comparable quality to state-of-the-art biocytin fillings, and [email protected] demonstrate feasibility of long term live cell imaging of human cells in vitro. -
Activation of Autophagy Rescues Synaptic and Cognitive Deficits in Fragile X Mice
Activation of autophagy rescues synaptic and cognitive deficits in fragile X mice Jingqi Yana,1, Morgan W. Porcha,1, Brenda Court-Vazqueza, Michael V. L. Bennetta,2, and R. Suzanne Zukina,2 aDominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, New York, NY 10461 Contributed by Michael V. L. Bennett, August 17, 2018 (sent for review May 29, 2018; reviewed by Claudia Bagni and Leonard K. Kaczmarek) Fragile X syndrome (FXS) is the most frequent form of heritable (17–19). Upon activation, mTOR phosphorylates Unc-51–like intellectual disability and autism. Fragile X (Fmr1-KO) mice exhibit autophagy-activating kinase 1 (ULK-1) at S757, a target of aberrant dendritic spine structure, synaptic plasticity, and cogni- mTORC1 and a well-established antiautophagy site (Fig. 1) tion. Autophagy is a catabolic process of programmed degradation (20). This, in turn, sequesters ULK-1 away from AMP kinase and recycling of proteins and cellular components via the lyso- (AMPK). AMPK phosphorylates and activates ULK-1 at S317. somal pathway. However, a role for autophagy in the pathophys- Upon activation, ULK-1 promotes phosphorylation and activa- iology of FXS is, as yet, unclear. Here we show that autophagic tion of Beclin-1 at S14, a critical step in the nucleation phase of flux, a functional readout of autophagy, and biochemical markers autophagy (21). Beclin-1 promotes lipidation of LC3-I to gen- of autophagy are down-regulated in hippocampal neurons of frag- erate its lipidated form LC3-II, enabling elongation of the lim- ile X mice. We further show that enhanced activity of mammalian iting membrane and the formation of autophagosomes (22). -
Spiking Neural Networks: Neuron Models, Plasticity, and Graph Applications
Virginia Commonwealth University VCU Scholars Compass Theses and Dissertations Graduate School 2015 Spiking Neural Networks: Neuron Models, Plasticity, and Graph Applications Shaun Donachy Virginia Commonwealth University Follow this and additional works at: https://scholarscompass.vcu.edu/etd Part of the Theory and Algorithms Commons © The Author Downloaded from https://scholarscompass.vcu.edu/etd/3984 This Thesis is brought to you for free and open access by the Graduate School at VCU Scholars Compass. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of VCU Scholars Compass. For more information, please contact [email protected]. c Shaun Donachy, July 2015 All Rights Reserved. SPIKING NEURAL NETWORKS: NEURON MODELS, PLASTICITY, AND GRAPH APPLICATIONS A Thesis submitted in partial fulfillment of the requirements for the degree of Master of Science at Virginia Commonwealth University. by SHAUN DONACHY B.S. Computer Science, Virginia Commonwealth University, May 2013 Director: Krzysztof J. Cios, Professor and Chair, Department of Computer Science Virginia Commonwealth University Richmond, Virginia July, 2015 TABLE OF CONTENTS Chapter Page Table of Contents :::::::::::::::::::::::::::::::: i List of Figures :::::::::::::::::::::::::::::::::: ii Abstract ::::::::::::::::::::::::::::::::::::: v 1 Introduction ::::::::::::::::::::::::::::::::: 1 2 Models of a Single Neuron ::::::::::::::::::::::::: 3 2.1 McCulloch-Pitts Model . 3 2.2 Hodgkin-Huxley Model . 4 2.3 Integrate and Fire Model . 6 2.4 Izhikevich Model . 8 3 Neural Coding Techniques :::::::::::::::::::::::::: 14 3.1 Input Encoding . 14 3.1.1 Grandmother Cell and Distributed Representations . 14 3.1.2 Rate Coding . 15 3.1.3 Sine Wave Encoding . 15 3.1.4 Spike Density Encoding . 15 3.1.5 Temporal Encoding . 16 3.1.6 Synaptic Propagation Delay Encoding . -
Plp-Positive Progenitor Cells Give Rise to Bergmann Glia in the Cerebellum
Citation: Cell Death and Disease (2013) 4, e546; doi:10.1038/cddis.2013.74 OPEN & 2013 Macmillan Publishers Limited All rights reserved 2041-4889/13 www.nature.com/cddis Olig2/Plp-positive progenitor cells give rise to Bergmann glia in the cerebellum S-H Chung1, F Guo2, P Jiang1, DE Pleasure2,3 and W Deng*,1,3,4 NG2 (nerve/glial antigen2)-expressing cells represent the largest population of postnatal progenitors in the central nervous system and have been classified as oligodendroglial progenitor cells, but the fate and function of these cells remain incompletely characterized. Previous studies have focused on characterizing these progenitors in the postnatal and adult subventricular zone and on analyzing the cellular and physiological properties of these cells in white and gray matter regions in the forebrain. In the present study, we examine the types of neural progeny generated by NG2 progenitors in the cerebellum by employing genetic fate mapping techniques using inducible Cre–Lox systems in vivo with two different mouse lines, the Plp-Cre-ERT2/Rosa26-EYFP and Olig2-Cre-ERT2/Rosa26-EYFP double-transgenic mice. Our data indicate that Olig2/Plp-positive NG2 cells display multipotential properties, primarily give rise to oligodendroglia but, surprisingly, also generate Bergmann glia, which are specialized glial cells in the cerebellum. The NG2 þ cells also give rise to astrocytes, but not neurons. In addition, we show that glutamate signaling is involved in distinct NG2 þ cell-fate/differentiation pathways and plays a role in the normal development of Bergmann glia. We also show an increase of cerebellar oligodendroglial lineage cells in response to hypoxic–ischemic injury, but the ability of NG2 þ cells to give rise to Bergmann glia and astrocytes remains unchanged. -
Neuron C Reference Guide Iii • Introduction to the LONWORKS Platform (078-0391-01A)
Neuron C Provides reference info for writing programs using the Reference Guide Neuron C programming language. 078-0140-01G Echelon, LONWORKS, LONMARK, NodeBuilder, LonTalk, Neuron, 3120, 3150, ShortStack, LonMaker, and the Echelon logo are trademarks of Echelon Corporation that may be registered in the United States and other countries. Other brand and product names are trademarks or registered trademarks of their respective holders. Neuron Chips and other OEM Products were not designed for use in equipment or systems, which involve danger to human health or safety, or a risk of property damage and Echelon assumes no responsibility or liability for use of the Neuron Chips in such applications. Parts manufactured by vendors other than Echelon and referenced in this document have been described for illustrative purposes only, and may not have been tested by Echelon. It is the responsibility of the customer to determine the suitability of these parts for each application. ECHELON MAKES AND YOU RECEIVE NO WARRANTIES OR CONDITIONS, EXPRESS, IMPLIED, STATUTORY OR IN ANY COMMUNICATION WITH YOU, AND ECHELON SPECIFICALLY DISCLAIMS ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of Echelon Corporation. Printed in the United States of America. Copyright © 2006, 2014 Echelon Corporation. Echelon Corporation www.echelon.com Welcome This manual describes the Neuron® C Version 2.3 programming language. It is a companion piece to the Neuron C Programmer's Guide. -
Control of Synapse Number by Glia Erik M
R EPORTS RGCs (8). Similar results were obtained un- der both conditions. After 2 weeks in culture, Control of Synapse Number we used whole-cell patch-clamp recording to measure the significant enhancement of spon- by Glia taneous synaptic activity by astrocytes (Fig. 1, A and B) (9). In the absence of astroglia, Erik M. Ullian,* Stephanie K. Sapperstein, Karen S. Christopherson, little synaptic activity occurred even when Ben A. Barres RGCs were cultured with their tectal target cells (6). This difference in synaptic activity Although astrocytes constitute nearly half of the cells in our brain, their persisted even after a month in culture, indi- function is a long-standing neurobiological mystery. Here we show by quantal cating that it is not accounted for by a matu- analyses, FM1-43 imaging, immunostaining, and electron microscopy that few rational delay. To examine whether glia reg- synapses form in the absence of glial cells and that the few synapses that do ulate synaptic activity by enhancing postsyn- form are functionally immature. Astrocytes increase the number of mature, aptic responsiveness, we measured the re- functional synapses on central nervous system (CNS) neurons by sevenfold and sponse of RGCs to pulses of L-glutamate are required for synaptic maintenance in vitro. We also show that most syn- applied to the cell somas. Regardless of the apses are generated concurrently with the development of glia in vivo. These presence of glia, RGCs responded with in- data demonstrate a previously unknown function for glia in inducing and ward currents (Fig. 1C) that were blocked by stabilizing CNS synapses, show that CNS synapse number can be profoundly glutamate receptor antagonists (10). -
Oligodendrocytes in Development, Myelin Generation and Beyond
cells Review Oligodendrocytes in Development, Myelin Generation and Beyond Sarah Kuhn y, Laura Gritti y, Daniel Crooks and Yvonne Dombrowski * Wellcome-Wolfson Institute for Experimental Medicine, Queen’s University Belfast, Belfast BT9 7BL, UK; [email protected] (S.K.); [email protected] (L.G.); [email protected] (D.C.) * Correspondence: [email protected]; Tel.: +0044-28-9097-6127 These authors contributed equally. y Received: 15 October 2019; Accepted: 7 November 2019; Published: 12 November 2019 Abstract: Oligodendrocytes are the myelinating cells of the central nervous system (CNS) that are generated from oligodendrocyte progenitor cells (OPC). OPC are distributed throughout the CNS and represent a pool of migratory and proliferative adult progenitor cells that can differentiate into oligodendrocytes. The central function of oligodendrocytes is to generate myelin, which is an extended membrane from the cell that wraps tightly around axons. Due to this energy consuming process and the associated high metabolic turnover oligodendrocytes are vulnerable to cytotoxic and excitotoxic factors. Oligodendrocyte pathology is therefore evident in a range of disorders including multiple sclerosis, schizophrenia and Alzheimer’s disease. Deceased oligodendrocytes can be replenished from the adult OPC pool and lost myelin can be regenerated during remyelination, which can prevent axonal degeneration and can restore function. Cell population studies have recently identified novel immunomodulatory functions of oligodendrocytes, the implications of which, e.g., for diseases with primary oligodendrocyte pathology, are not yet clear. Here, we review the journey of oligodendrocytes from the embryonic stage to their role in homeostasis and their fate in disease. We will also discuss the most common models used to study oligodendrocytes and describe newly discovered functions of oligodendrocytes. -
Chapter 8 Nervous System
Chapter 8 Nervous System I. Functions A. Sensory Input – stimuli interpreted as touch, taste, temperature, smell, sound, blood pressure, and body position. B. Integration – CNS processes sensory input and initiates responses categorizing into immediate response, memory, or ignore C. Homeostasis – maintains through sensory input and integration by stimulating or inhibiting other systems D. Mental Activity – consciousness, memory, thinking E. Control of Muscles & Glands – controls skeletal muscle and helps control/regulate smooth muscle, cardiac muscle, and glands II. Divisions of the Nervous system – 2 anatomical/main divisions A. CNS (Central Nervous System) – consists of the brain and spinal cord B. PNS (Peripheral Nervous System) – consists of ganglia and nerves outside the brain and spinal cord – has 2 subdivisions 1. Sensory Division (Afferent) – conducts action potentials from PNS toward the CNS (by way of the sensory neurons) for evaluation 2. Motor Division (Efferent) – conducts action potentials from CNS toward the PNS (by way of the motor neurons) creating a response from an effector organ – has 2 subdivisions a. Somatic Motor System – controls skeletal muscle only b. Autonomic System – controls/effects smooth muscle, cardiac muscle, and glands – 2 branches • Sympathetic – accelerator “fight or flight” • Parasympathetic – brake “resting and digesting” * 4 Types of Effector Organs: skeletal muscle, smooth muscle, cardiac muscle, and glands. III. Cells of the Nervous System A. Neurons – receive stimuli and transmit action potentials -
Area-Specific Synapse Structure in Branched Posterior Nucleus Axons Reveals a New Level of Complexity in Thalamocortical Networks
The Journal of Neuroscience, March 25, 2020 • 40(13):2663–2679 • 2663 Systems/Circuits Area-Specific Synapse Structure in Branched Posterior Nucleus Axons Reveals a New Level of Complexity in Thalamocortical Networks Javier Rodriguez-Moreno,1 Cesar Porrero,1 Astrid Rollenhagen,2 Mario Rubio-Teves,1 Diana Casas-Torremocha,1 X Lidia Alonso-Nanclares,3 Rachida Yakoubi,2 XAndrea Santuy,3 XAngel Merchan-Pe´rez,3,5,6 XJavier DeFelipe,3,4,5 Joachim H.R. Lu¨bke,2,7,8* and XFrancisco Clasca1* 1Department of Anatomy and Neuroscience, School of Medicine, Auto´noma de Madrid University, 28029 Madrid, Spain, 2Institute of Neuroscience and Medicine INM-10, Research Centre Ju¨lich GmbH, 52425 Ju¨lich, Germany, 3Laboratorio Cajal de Circuitos Corticales, Centro de Tecnología Biome´dica, Universidad Polite´cnica de Madrid, Pozuelo de Alarco´n, 28223 Madrid, Spain, 4Instituto Cajal, Consejo Superior de Investigaciones Científicas, Arce 37 28002, Madrid, Spain, 5CIBERNED, Centro de Investigacio´n Biome´dica en Red de Enfermedades Neurodegenerativas, 28031 Madrid, Spain, 6Departamento de Arquitectura y Tecnología de Sistemas Informa´ticos, Universidad Polite´cnica de Madrid. Boadilla del Monte, 28660 Madrid, Spain, 7Department of Psychiatry, Psychotherapy and Psychosomatics, Medical Faculty RWTH University Hospital Aachen, 52074 Aachen, Germany, and 8JARA-Translational Brain Medicine, 52425 Ju¨lich-Aachen, Germany Thalamocortical posterior nucleus (Po) axons innervating the vibrissal somatosensory (S1) and motor (MC) cortices are key links in the brain neuronal network that allows rodents to explore the environment whisking with their motile snout vibrissae. Here, using fine-scale high-end 3D electron microscopy, we demonstrate in adult male C57BL/6 wild-type mice marked differences between MC versus S1 Po synapses in (1) bouton and active zone size, (2) neurotransmitter vesicle pool size, (3) distribution of mitochondria around synapses, and (4) proportion of synapses established on dendritic spines and dendritic shafts. -
The Interplay Between Neurons and Glia in Synapse Development And
Available online at www.sciencedirect.com ScienceDirect The interplay between neurons and glia in synapse development and plasticity Jeff A Stogsdill and Cagla Eroglu In the brain, the formation of complex neuronal networks and regulate distinct aspects of synaptic development and amenable to experience-dependent remodeling is complicated circuit connectivity. by the diversity of neurons and synapse types. The establishment of a functional brain depends not only on The intricate communication between neurons and glia neurons, but also non-neuronal glial cells. Glia are in and their cooperative roles in synapse formation are now continuous bi-directional communication with neurons to direct coming to light due in large part to advances in genetic the formation and refinement of synaptic connectivity. This and imaging tools. This article will examine the progress article reviews important findings, which uncovered cellular made in our understanding of the role of mammalian and molecular aspects of the neuron–glia cross-talk that perisynaptic glia (astrocytes and microglia) in synapse govern the formation and remodeling of synapses and circuits. development, maturation, and plasticity since the previ- In vivo evidence demonstrating the critical interplay between ous Current Opinion article [1]. An integration of past and neurons and glia will be the major focus. Additional attention new findings of glial control of synapse development and will be given to how aberrant communication between neurons plasticity is tabulated in Box 1. and glia may contribute to neural pathologies. Address Glia control the formation of synaptic circuits Department of Cell Biology, Duke University Medical Center, Durham, In the CNS, glial cells are in tight association with NC 27710, USA synapses in all brain regions [2]. -
Neuron Morphology Influences Axon Initial Segment Plasticity1,2,3
New Research Neuronal Excitability Neuron Morphology Influences Axon Initial Segment Plasticity1,2,3 Allan T. Gulledge1 and Jaime J. Bravo2 DOI:http://dx.doi.org/10.1523/ENEURO.0085-15.2016 1Department of Physiology and Neurobiology, Geisel School of Medicine at Dartmouth, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire 03756, and 2Thayer School of Engineering at Dartmouth, Hanover, New Hampshire 03755 Visual Abstract In most vertebrate neurons, action potentials are initiated in the axon initial segment (AIS), a specialized region of the axon containing a high density of voltage-gated sodium and potassium channels. It has recently been proposed that neurons use plasticity of AIS length and/or location to regulate their intrinsic excitability. Here we quantify the impact of neuron morphology on AIS plasticity using computational models of simplified and realistic somatodendritic morphologies. In small neurons (e.g., den- tate granule neurons), excitability was highest when the AIS was of intermediate length and located adjacent to the soma. Conversely, neu- rons having larger dendritic trees (e.g., pyramidal neurons) were most excitable when the AIS was longer and/or located away from the soma. For any given somatodendritic morphology, increasing dendritic mem- brane capacitance and/or conductance favored a longer and more distally located AIS. Overall, changes to AIS length, with corresponding changes in total sodium conductance, were far more effective in regulating neuron excitability than were changes in AIS location, while dendritic capacitance had a larger impact on AIS performance than did dendritic conductance. The somatodendritic influence on AIS performance reflects modest soma- to-AIS voltage attenuation combined with neuron size-dependent changes in AIS input resistance, effective membrane time constant, and isolation from somatodendritic capacitance.