Brain Plasticity and Behaviour in the Developing Brain
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Neuromodulators and Long-Term Synaptic Plasticity in Learning and Memory: a Steered-Glutamatergic Perspective
brain sciences Review Neuromodulators and Long-Term Synaptic Plasticity in Learning and Memory: A Steered-Glutamatergic Perspective Amjad H. Bazzari * and H. Rheinallt Parri School of Life and Health Sciences, Aston University, Birmingham B4 7ET, UK; [email protected] * Correspondence: [email protected]; Tel.: +44-(0)1212044186 Received: 7 October 2019; Accepted: 29 October 2019; Published: 31 October 2019 Abstract: The molecular pathways underlying the induction and maintenance of long-term synaptic plasticity have been extensively investigated revealing various mechanisms by which neurons control their synaptic strength. The dynamic nature of neuronal connections combined with plasticity-mediated long-lasting structural and functional alterations provide valuable insights into neuronal encoding processes as molecular substrates of not only learning and memory but potentially other sensory, motor and behavioural functions that reflect previous experience. However, one key element receiving little attention in the study of synaptic plasticity is the role of neuromodulators, which are known to orchestrate neuronal activity on brain-wide, network and synaptic scales. We aim to review current evidence on the mechanisms by which certain modulators, namely dopamine, acetylcholine, noradrenaline and serotonin, control synaptic plasticity induction through corresponding metabotropic receptors in a pathway-specific manner. Lastly, we propose that neuromodulators control plasticity outcomes through steering glutamatergic transmission, thereby gating its induction and maintenance. Keywords: neuromodulators; synaptic plasticity; learning; memory; LTP; LTD; GPCR; astrocytes 1. Introduction A huge emphasis has been put into discovering the molecular pathways that govern synaptic plasticity induction since it was first discovered [1], which markedly improved our understanding of the functional aspects of plasticity while introducing a surprisingly tremendous complexity due to numerous mechanisms involved despite sharing common “glutamatergic” mediators [2]. -
Review Article Mechanisms of Cerebrovascular Autoregulation and Spreading Depolarization-Induced Autoregulatory Failure: a Literature Review
Int J Clin Exp Med 2016;9(8):15058-15065 www.ijcem.com /ISSN:1940-5901/IJCEM0026645 Review Article Mechanisms of cerebrovascular autoregulation and spreading depolarization-induced autoregulatory failure: a literature review Gang Yuan1*, Bingxue Qi2*, Qi Luo1 1Department of Neurosurgery, The First Hospital of Jilin University, Changchun, China; 2Department of Endocrinology, Jilin Province People’s Hospital, Changchun, China. *Equal contributors. Received February 25, 2016; Accepted June 4, 2016; Epub August 15, 2016; Published August 30, 2016 Abstract: Cerebrovascular autoregulation maintains brain hemostasis via regulating cerebral flow when blood pres- sure fluctuation occurs. Monitoring autoregulation can be achieved by transcranial Doppler ultrasonography, the pressure reactivity index (PRx) can serve as a secondary index of vascular deterioration, and outcome and prognosis are assessed by the low-frequency PRx. Although great changes in arterial blood pressure (ABP) occur, complex neu- rogenic, myogenic, endothelial, and metabolic mechanisms are involved to maintain the flow within its narrow limits. The steady association between ABP and cerebral blood flow (CBF) reflects static cerebral autoregulation (CA). Spreading depolarization (SD) is a sustained depolarization of neurons with concomitant pronounced breakdown of ion gradients, which originates in patients with brain ischemia, hemorrhage, trauma, and migraine. It is character- ized by the propagation of an extracellular negative potential, followed by an increase in O2 and glucose consump- tion. Immediately after SD, CA is transiently impaired but is restored after 35 min. This process initiates a cascade of pathophysiological mechanisms, leading to neuronal damage and loss if consecutive events are evoked. The clini- cal application of CA in regulating CBF is to dilate the cerebral arteries as a compensatory mechanism during low blood pressure, thus protecting the brain from ischemia. -
Long-Term Potentiation and Long-Term Depression of Primary Afferent Neurotransmission in the Rat Spinal Cord
The Journal of Neuroscience, December 1993. 13(12): 52286241 Long-term Potentiation and Long-term Depression of Primary Afferent Neurotransmission in the Rat Spinal Cord M. RandiC, M. C. Jiang, and R. Cerne Department of Veterinary Physiology and Pharmacology, Iowa State University, Ames, Iowa 50011 Synaptic transmission between dorsal root afferents and ably mediated by L-glutamate, or a related amino acid (Jahr and neurons in the superficial laminae of the spinal dorsal horn Jessell, 1985; Gerber and RandiC, 1989; Kangrga and Randic, (laminae I-III) was examined by intracellular recording in a 1990, 1991; Yoshimura and Jessell, 1990; Ceme et al., 1991). transverse slice preparation of rat spinal cord. Brief high- Neuronal excitatory amino acids (EAAs), including gluta- frequency electrical stimulation (300 pulses at 100 Hz) of mate, produce their effects through two broad categoriesof re- primary afferent fibers produced a long-term potentiation ceptors called ionotropic and metabotropic (Honor6 et al., 1988; (LTP) or a long-term depression (LTD) of fast (monosynaptic Schoepp et al., 1991; Watkins et al., 1990). The ionotropic and polysynaptic) EPSPs in a high proportion of dorsal horn NMDA, a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic neurons. Both the AMPA and the NMDA receptor-mediated acid (AMPA)/quisqualate (QA), and kainate receptors directly components of synaptic transmission at the primary afferent regulate the opening of ion channelsto Na, K+, and, in the case synapses with neurons in the dorsal horn can exhibit LTP of NMDA receptors, CaZ+as well (Mayer and Westbrook, 1987; and LTD of the synaptic responses. In normal and neonatally Ascher and Nowak, 1987). -
Cerebral Pressure Autoregulation in Traumatic Brain Injury
Neurosurg Focus 25 (4):E7, 2008 Cerebral pressure autoregulation in traumatic brain injury LEONARDO RANGE L -CASTIL L A , M.D.,1 JAI M E GAS C O , M.D. 1 HARING J. W. NAUTA , M.D., PH.D.,1 DAVID O. OKONK W O , M.D., PH.D.,2 AND CLUDIAA S. ROBERTSON , M.D.3 1Division of Neurosurgery, University of Texas Medical Branch, Galveston; 3Department of Neurosurgery, Baylor College of Medicine, Houston, Texas; and 2Department of Neurosurgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania An understanding of normal cerebral autoregulation and its response to pathological derangements is helpful in the diagnosis, monitoring, management, and prognosis of severe traumatic brain injury (TBI). Pressure autoregula- tion is the most common approach in testing the effects of mean arterial blood pressure on cerebral blood flow. A gold standard for measuring cerebral pressure autoregulation is not available, and the literature shows considerable disparity in methods. This fact is not surprising given that cerebral autoregulation is more a concept than a physically measurable entity. Alterations in cerebral autoregulation can vary from patient to patient and over time and are critical during the first 4–5 days after injury. An assessment of cerebral autoregulation as part of bedside neuromonitoring in the neurointensive care unit can allow the individualized treatment of secondary injury in a patient with severe TBI. The assessment of cerebral autoregulation is best achieved with dynamic autoregulation methods. Hyperven- tilation, hyperoxia, nitric oxide and its derivates, and erythropoietin are some of the therapies that can be helpful in managing cerebral autoregulation. In this review the authors summarize the most important points related to cerebral pressure autoregulation in TBI as applied in clinical practice, based on the literature as well as their own experience. -
All-Trans Retinoic Acid Induces Synaptic Plasticity in Human Cortical Neurons
bioRxiv preprint doi: https://doi.org/10.1101/2020.09.04.267104; this version posted September 4, 2020. 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. All-Trans Retinoic Acid induces synaptic plasticity in human cortical neurons Maximilian Lenz1, Pia Kruse1, Amelie Eichler1, Julia Muellerleile2, Jakob Straehle3, Peter Jedlicka2,4, Jürgen Beck3,5, Thomas Deller2, Andreas Vlachos1,5,*. 1Department of Neuroanatomy, Institute of Anatomy and Cell Biology, Faculty of Medicine, University of Freiburg, Germany. 2Institute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University Frankfurt, Germany. 3Department of Neurosurgery, Medical Center and Faculty of Medicine, University of Freiburg, Germany. 4ICAR3R - Interdisciplinary Centre for 3Rs in Animal Research, Faculty of Medicine, Justus-Liebig- University, Giessen, Germany. 5Center for Basics in Neuromodulation (NeuroModulBasics), Faculty of Medicine, University of Freiburg, Germany. Abbreviated title: Synaptic plasticity in human cortex *Correspondence to: Andreas Vlachos, M.D. Albertstr. 17 79104 Freiburg, Germany Phone: +49 (0)761 203 5056 Fax: +49 (0)761 203 5054 Email: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.09.04.267104; this version posted September 4, 2020. 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. ABSTRACT A defining feature of the brain is its ability to adapt structural and functional properties of synaptic contacts in an experience-dependent manner. In the human cortex direct experimental evidence for synaptic plasticity is currently missing. -
SHORT-TERM SYNAPTIC PLASTICITY Robert S. Zucker Wade G. Regehr
23 Jan 2002 14:1 AR AR148-13.tex AR148-13.SGM LaTeX2e(2001/05/10) P1: GJC 10.1146/annurev.physiol.64.092501.114547 Annu. Rev. Physiol. 2002. 64:355–405 DOI: 10.1146/annurev.physiol.64.092501.114547 Copyright c 2002 by Annual Reviews. All rights reserved SHORT-TERM SYNAPTIC PLASTICITY Robert S. Zucker Department of Molecular and Cell Biology, University of California, Berkeley, California 94720; e-mail: [email protected] Wade G. Regehr Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115; e-mail: [email protected] Key Words synapse, facilitation, post-tetanic potentiation, depression, augmentation, calcium ■ Abstract Synaptic transmission is a dynamic process. Postsynaptic responses wax and wane as presynaptic activity evolves. This prominent characteristic of chemi- cal synaptic transmission is a crucial determinant of the response properties of synapses and, in turn, of the stimulus properties selected by neural networks and of the patterns of activity generated by those networks. This review focuses on synaptic changes that re- sult from prior activity in the synapse under study, and is restricted to short-term effects that last for at most a few minutes. Forms of synaptic enhancement, such as facilitation, augmentation, and post-tetanic potentiation, are usually attributed to effects of a resid- 2 ual elevation in presynaptic [Ca +]i, acting on one or more molecular targets that appear to be distinct from the secretory trigger responsible for fast exocytosis and phasic release of transmitter to single action potentials. We discuss the evidence for this hypothesis, and the origins of the different kinetic phases of synaptic enhancement, as well as the interpretation of statistical changes in transmitter release and roles played by other 2 2 factors such as alterations in presynaptic Ca + influx or postsynaptic levels of [Ca +]i. -
Synaptic Plasticity: Understanding the Neurobiological Mechanisms of Learning and Memory
www.medigraphic.org.mx ACTUALIZACION POR TEMAS SYNAPTIC PLASTICITY: UNDERSTANDING THE NEUROBIOLOGICAL MECHANISMS OF LEARNING AND MEMORY. PART I Philippe Leff,1 Héctor Romo-Parra,2 Mayra Medécigo,1 Rafael Gutiérrez,2 Benito Anton1 SUMMARY RESUMEN Plasticity of the nervous system has been related to learning and Uno de los fenómenos más interesantes dentro del campo de la memory processing as early as the beginning of the century; although, neurobiología, es el fenómeno de la plasticidad cerebral relacionada remotely, brain plasticity in relation to behavior has been connoted con los eventos de aprendizaje y el procesamiento del fenómeno de over the past two centuries. However, four decades ago, several memoria. De hecho, estos fenómenos neurobiológicos empezaron evidences have shown that experience and training induce neural a ser estudiados desde principios de siglo. Remotamente, el fenóme- changes, showing that major neuroanatomical, neurochemical as no de plasticidad cerebral en relación con el desarrollo y aprendiza- well as molecular changes are required for the establishment of a je de las conductas fue ya concebido y cuestionado desde hace más long-term memory process. Early experimental procedures showed de dos centurias. Sin embargo, desde hace cuatro décadas, múltiples that differential experience, training and/or informal experience evidencias experimentales han demostrado que tanto la experiencia could produce altered quantified changes in the brain of mammals. o el entrenamiento en la ejecución de tareas operantes aprendidas, Moreover, neuropsychologists have emphasized that different inducen cambios plásticos en la fisiología neuronal, incluyendo los memories could be localized in separate cortical areas of the brain, cambios neuroquímicos y moleculares que se requieren para conso- but updated evidences assert that memory systems are specifically lidar una memoria a largo plazo. -
Brenda Milner 276
EDITORIAL ADVISORY COMMITTEE Verne S. Caviness Bernice Grafstein Charles G. Gross Theodore Melnechuk Dale Purves Gordon M. Shepherd Larry W. Swanson (Chairperson) The History of Neuroscience in Autobiography VOLUME 2 Edited by Larry R. Squire ACADEMIC PRESS San Diego London Boston New York Sydney Tokyo Toronto This book is printed on acid-free paper. @ Copyright 91998 by The Society for Neuroscience All Rights Reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher. Academic Press a division of Harcourt Brace & Company 525 B Street, Suite 1900, San Diego, California 92101-4495, USA http://www.apnet.com Academic Press 24-28 Oval Road, London NW1 7DX, UK http://www.hbuk.co.uk/ap/ Library of Congress Catalog Card Number: 98-87915 International Standard Book Number: 0-12-660302-2 PRINTED IN THE UNITED STATES OF AMERICA 98 99 00 01 02 03 EB 9 8 7 6 5 4 3 2 1 Contents Lloyd M. Beidler 2 Arvid Carlsson 28 Donald R. Griffin 68 Roger Guillemin 94 Ray Guillery 132 Masao Ito 168 Martin G. Larrabee 192 Jerome Lettvin 222 Paul D. MacLean 244 Brenda Milner 276 Karl H. Pribram 306 Eugene Roberts 350 Gunther Stent 396 Brenda Milner BORN: Manchester, England July 15, 1918 EDUCATION: University of Cambridge, B.A. (1939) University of Cambridge, M.A. (1949) McGill University, Ph.D. (1952) University of Cambridge, Sc.D. (1972) APPOINTMENTS" Universit~ de Montreal (1944) McGill University (1952) HONORS AND AWARDS: (SELECTED): Distinguished Scientific Contribution Award, American Psychological Association (1973) Fellow, Royal Society of Canada (1976) Foreign Associate, National Academy of Sciences U.S.A. -
([PDF]) an Introduction to Brain and Behavior READ ONLINE by Bryan Kolb
Overview book of An Introduction to Brain and Behavior From authors Bryan Kolb and Ian Whishaw, and new coauthor G. Campbell Teskey, An Introduction to Brain and Behavior offers a unique inquiry-based introduction to behavioral neuroscience, with each chapter focusing on a central question (i.e., "How Does the Nervous System Function?"). It also incorporates a distinctive clinical perspective, with examples showing students what happens when common neuronal processes malfunction. Now this acclaimed book returns in a thoroughly up-to-date new edition.Founders of a prestigious neuroscience institute at the University of Lethbridge in Alberta, Canada, Kolb and Whishaw are renowned as both active scientists and teachers. G. Campbell Teskey of the University of Calgary, also brings to the book a wealth of experience as a researcher and educator. Together, they are the ideal author team for guiding students from a basic understanding the biology of behavior to the very frontiers of some of the most exciting and impactful research being conducted today. The new edition also has its own dedicated version of Worth Publishers’ breakthrough online course space, LaunchPad, giving it the most robust media component of any textbook for the course. An Introduction to Brain and Behavior by Bryan Kolb An Introduction to Brain and Behavior Epub An Introduction to Brain and Behavior Download vk An Introduction to Brain and Behavior Download ok.ru An Introduction to Brain and Behavior Download Youtube An Introduction to Brain and Behavior Download Dailymotion -
Chapter 11: Synaptic Plasticity (PDF)
11 SYNAPTIC PLASTICITY ROBERT C. MALENKA The most fascinating and important property of the mam- SHORT-TERM SYNAPTIC PLASTICITY malian brain is its remarkable plasticity, which can be thought of as the ability of experience to modify neural Virtually every synapse that has been examined in organisms circuitry and thereby to modify future thought, behavior, ranging from simple invertebrates to mammals exhibits nu- and feeling. Thinking simplistically, neural activity can merous different forms of short-term synaptic plasticity that modify the behavior of neural circuits by one of three mech- last on the order of milliseconds to a few minutes (for de- anisms: (a) by modifying the strength or efficacy of synaptic tailed reviews, see 1 and 2). In general, these result from a transmission at preexisting synapses, (b) by eliciting the short-lasting modulation of transmitter release that can growth of new synaptic connections or the pruning away occur by one of two general types of mechanisms. One of existing ones, or (c) by modulating the excitability prop- involves a change in the amplitude of the transient rise in erties of individual neurons. Synaptic plasticity refers to the intracellular calcium concentration that occurs when an ac- first of these mechanisms, and for almost 100 years, activity- tion potential invades a presynaptic terminal. This occurs dependent changes in the efficacy of synaptic communica- because of some modification in the calcium influx before tion have been proposed to play an important role in the transmitter release or because the basal level of calcium in remarkable capacity of the brain to translate transient expe- the presynaptic terminal has been elevated because of prior riences into seemingly infinite numbers of memories that activity at the terminal. -
Fundamentals of Human Neuropsychology, 6Th Edition by Bryan Kolb and Ian Q
The Journal of Undergraduate Neuroscience Education (JUNE), Spring 2008, 6(2):R3-R4 TEXTBOOK REVIEW Fundamentals of Human Neuropsychology, 6th Edition By Bryan Kolb and Ian Q. Whishaw Reviewed by Gina A. Mollet Department of Psychology, Adams State College, Alamosa, CO 81102 Kolb and Whishaw’s Fundamentals of Human researchers might approach the same problem and they Neuropsychology is an excellent textbook for use in upper are exposed to a variety of research in the fields of division behavioral neuroscience or neuropsychology neuroscience. courses. It begins by providing an excellent history of At times I did find it difficult to get through the detailed neuropsychology and continues to explain the neural descriptions of the research experiments. Also, I mechanisms that underlie simple and complex behaviors. sometimes felt overwhelmed with the sheer number of The book is divided into five parts that each address a research experiments that were summarized in the text. different aspect of brain functioning. Part I describes the For example, in Chapter 9 there are several descriptions of history and development of neuropsychology, anatomy of experiments where single cell recordings were used in the neuron and brain, how communication occurs in the monkey’s performing specific types of movements. As I neuron, the influence of drugs on behavior, and imaging read the experiments, it was difficult to imagine exactly methods. Part II focuses on the organization of the cortex, how the experiment was conducted. To alleviate this the sensory systems, and the motor system. Part III problem, the text includes excellent images of the examines each lobe of the brain and disconnection behavioral tasks used in the research and the cellular syndromes. -
Dr. Majid Mohajerani Named First Recipient of Dr. Bryan Kolb Professorship/Chair in Neuroscience
For immediate release — Thursday, October 29, 2020 Dr. Majid Mohajerani named first recipient of Dr. Bryan Kolb Professorship/Chair in Neuroscience A new professorship created at the University of Lethbridge honours the legacy of one of the most influential figures in establishing the study of neuroscience and neuropsychology. It’s first appointee is a rising star who continues to push the boundaries of the field. Dr. Majid Mohajerani has been named the first recipient of the Dr. Bryan Kolb Professorship/Chair in Neuroscience, which carries a five-year term that may be renewed once for a second five- year term. The award is an endorsement of the outstanding research Mohajerani has conducted since joining the U of L as part of the Government of Alberta’s Campus Alberta Innovation Program (CAIP) Chairs plan in 2014. At the time, Mohajerani had been serving as a research associate at the International School for Advanced Studies in Trieste, Italy and at the University of British Columbia, and selected the U of L above a number of suitors. “This is a very important appointment for the University and the Department of Neuroscience,” says the U of L’s Dr. Erasmus Okine, provost and vice-president (academic). “Majid’s advanced work, primarily associated with the study of cognitive decline and Alzheimer’s disease, has led to a better understanding of how the brain ages and the underlying biological processes associated with the development of Alzheimer’s disease. He continues to attract significant research funding support and push the boundaries of his field as well as the reputation of the Canadian Centre for Behavioural Neuroscience (CCBN).” Mohajerani studies the neural basis of memory and its disorders.