DOCSLIB.ORG

The Contribution of Ion Channels in Input-Output Plasticity Dominique Debanne, Michaël Russier

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Contribution of Ion Channels in Input-Output Plasticity Dominique Debanne, Michaël Russier The contribution of ion channels in input-output plasticity Dominique Debanne, Michaël Russier To cite this version: Dominique Debanne, Michaël Russier. The contribution of ion channels in input-output plasticity. Neurobiology of Learning and Memory, Elsevier, 2019, 10.1016/j.nlm.2019.107095. hal-02363603 HAL Id: hal-02363603 https://hal-amu.archives-ouvertes.fr/hal-02363603 Submitted on 14 Nov 2019 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Neurobiology of Learning and Memory 166 (2019) 107095 Contents lists available at ScienceDirect Neurobiology of Learning and Memory journal homepage: www.elsevier.com/locate/ynlme The contribution of ion channels in input-output plasticity T ⁎ Dominique Debanne , Michaël Russier UNIS, UMR1072 INSERM – AMU, Marseille, France ARTICLE INFO ABSTRACT Keywords: Persistent changes that occur in brain circuits are classically thought to be mediated by long-term modifications Ion channels in synaptic efficacy. Yet, many studies have shown that voltage-gated ion channels located at the input and Activity-dependent plasticity output side of the neurons are also the subject to persistent modifications. These channels are thus responsible Learning for intrinsic plasticity that is expressed in many different neuronal types including glutamatergic principal Memory neurons and GABAergic interneurons. As for synaptic plasticity, activation of synaptic glutamate receptors in- LTP itiate persistent modification in neuronal excitability. We review here how synaptic input can be efficiently LTD fi STDP altered by activity-dependent modulation of ion channels that control EPSP ampli cation, spike threshold or resting membrane potential. We discuss the nature of the learning rules shared by intrinsic and synaptic plas- ticity, the mechanisms of ion channel regulation and the impact of intrinsic plasticity on induction of synaptic modifications. 1. Introduction dependent plasticity (STDP) rule (Abbott & Nelson, 2000; Feldman, 2012) in which positive correlation between excitatory post-synaptic Information storage in the brain is classically thought to result from potentials (EPSPs) and single spikes led to LTP whereas their negative long-lasting modifications of chemical synaptic transmission. Support correlation led to LTD (Bi & Poo, 1998; Debanne, Gahwiler, & to this has been provided by many studies showing up- or down-reg- Thompson, 1998; Feldman, 2000; Markram, Lubke, Frotscher, & ulation of synaptic transmission following specific regimes of synaptic Sakmann, 1997). activity. For instance, long-term synaptic potentiation (LTP) occurs All these synaptic modifications are specific to the synapse stimu- following high frequency stimulation of afferent glutamatergic inputs at lated during the cellular conditioning (Bliss & Collingridge, 1993; many synaptic pathways including the Schaffer collateral-CA1 cell sy- Debanne, Gahwiler, & Thompson, 1994; Malenka, 1991) and may thus napse (Bliss & Collingridge, 1993; Malenka, 1991), mossy-fibre-CA3 allow high capacity of information storage. However, synaptic plasti- cell synapse (Zalutsky & Nicoll, 1990), visual neocortical inputs (Artola city appears to not constitute the sole manner to modify input-output & Singer, 1987), and glutamatergic afferents to inhibitory interneurons function and voltage-gated channels located at the input and output (Lamsa, Heeroma, Somogyi, Rusakov, & Kullmann, 2007). Long-term sides of neurons are also subject to activity-dependent modification synaptic depression (LTD) is induced homosynaptically following low (Debanne, Inglebert, & Russier, 2019; Titley, Brunel, & Hansel, 2017; frequency stimulation of glutamatergic inputs. Evidence for homo- Zhang & Linden, 2003). Here, we review recent in vitro works devoted synaptic LTD has been provided at the Schaffer collateral-CA1 cell sy- to the role of ion channels in the modulation of input-output function in napse (Dudek & Bear, 1992; Mulkey & Malenka, 1992), inputs to visual mammalian neurons. First, we will consider the different ways of cortical neurons (Kirkwood, Dudek, Gold, Aizenman, & Bear, 1993). modulating input-output function at the neuronal scale. Then, we will LTP and LTD have been shown to be induced associatively when a sy- review the learning rules of input-output plasticity on the basis of those naptic input is paired with postsynaptic spiking activity. LTP is induced defined for synaptic modifications. Finally, we will discuss intrinsic at Schaffer collateral inputs when glutamatergic input is synchronously plasticity in GABAergic interneurons, the impact of ion channel reg- paired with burst of action potentials (Gustafsson, Wigstrom, Abraham, ulation on induction of synaptic plasticity and intrinsic plasticity in vivo. & Huang, 1987; Kelso, Ganong, & Brown, 1986; Sastry, Goh, & Auyeung, 1986) whereas LTD results of asynchronous activation of 2. Activity-dependent modulation in input-output function these two stimuli (Debanne et al., 1994, 1996). These forms of asso- ciative synaptic plasticity led to the emergence of the spike-timing- Input-output function is a critical operation at the neuronal scale ⁎ Corresponding author. E-mail address: [email protected] (D. Debanne). https://doi.org/10.1016/j.nlm.2019.107095 Received 19 June 2019; Received in revised form 4 September 2019; Accepted 16 September 2019 Available online 17 September 2019 1074-7427/ © 2019 Published by Elsevier Inc. D. Debanne and M. Russier Neurobiology of Learning and Memory 166 (2019) 107095 AB (Magee, 1999). These channels are activated at resting membrane po- Synaptic plasticity Amplified EPSP tential and attenuate EPSP amplitude through their deactivation. Thus, any modulation of h-channels may increase or decrease EPSP-spike coupling (Gastrein et al., 2011). The down-regulation of these channels EPSC EPSC HCN, Kv4 have been shown to enhance EPSP summation (Wang, Xu, Wu, Duan, & Poo, 2003) and input-output function (Campanac, Daoudal, Ankri, & Debanne, 2008) following LTP induction. Kv4.2 is another voltage- gated ion channel located in the dendrites that attenuates both EPSP amplitude and back-propagating action potentials in distal dendrites (Hoffman, Magee, Colbert, & Johnston, 1997). The down-regulation of EPSP Kv4.2 channel activity results in enhancement of both EPSP amplitude C D and local back-propagation (Frick, Magee, & Johnston, 2004; Kim, Jung, Clemens, Petralia, & Hoffman, 2007). As synaptic plasticity, the Threshold modulation Depolarized resting potential modulation of EPSP amplification is generally local as other inputs re- main unchanged (Campanac & Debanne, 2008; Wang et al., 2003). + EPSC EPSC EPSPs are also shaped by small conductance calcium-activated K (SK) HCN, Na/K ATPase channels. Calcium influx through NMDAR has been shown to activate SK channels located in the dendritic spines thus attenuating EPSP am- plitude and duration (Adelman, Maylie, & Sah, 2012; Faber, Delaney, & Sah, 2005; Ngo-Anh et al., 2005). Interestingly, SK channels are Nav, Kv1 downregulated following stimulation of synaptic metabotropic gluta- mate receptor subtype 5 (mGluR5) resulting in enhancement of EPSP- Fig. 1. Multiple mechanisms of input-output plasticity. (A) Synaptic contribu- spike coupling (Sourdet, Russier, Daoudal, Ankri, & Debanne, 2003). tion to input-output modulation. Potentiation of synaptic transmission through an increase in transmitter release and/or postsynaptic receptor density is Nevertheless, EPSP-spike coupling in cortical neurons is poorly de- characterized by an enhanced excitatory post-synaptic current (EPSC). At the termined by EPSP amplitude and highly dependent on the rate and the axon initial segment (AIS), the excitatory post-synaptic potential (EPSP) be- waveform of dendritic EPSPs (Larkum, Zhu, & Sakmann, 2001). In comes large enough to cross the action potential (AP) threshold. As synaptic cerebellar Purkinje cells, EPSP amplitude has also limited control over strength is regulated, EPSP slope is enhanced. (B) Change in EPSP amplifica- cell firing but pharmacological modulation of SK channel and SK-de- tion. When dendritic HCN or Kv4 channels (green) are regulated, the resulting pendent plasticity strongly regulate spike firing (Ohtsuki & Hansel, EPSP is amplified and crosses the spike threshold. Note that here the synaptic 2018). current (EPSC) is kept constant to clearly distinguish intrinsic from synaptic changes and the initial EPSP slope remains unchanged. These first two mod- ifications (A & B) are local because they do not affect all synaptic inputs. (C) 2.2. Modulation of spike threshold Change in spike threshold. Spike firing increases as a result of hyperpolarization of AP threshold by the regulation of voltage-gated ion channels (Nav or Kv1) located at the AIS. Here again, the excitatory synaptic current (EPSC) remains Input-output function may also be altered via modulation of ion + unchanged. (D) Depolarization of resting membrane potential. Following channels that control the spike threshold (Fig. 1C). Voltage-gated Na + modulation of voltage-gated channels (HCN) or ion pumps
Load more

Recommended publications
  • Rab3a As a Modulator of Homeostatic Synaptic Plasticity
    Wright State University CORE Scholar Browse all Theses and Dissertations Theses and Dissertations 2014 Rab3A as a Modulator of Homeostatic Synaptic Plasticity Andrew G. Koesters Wright State University Follow this and additional works at: https://corescholar.libraries.wright.edu/etd_all Part of the Biomedical Engineering and Bioengineering Commons Repository Citation Koesters, Andrew G., "Rab3A as a Modulator of Homeostatic Synaptic Plasticity" (2014). Browse all Theses and Dissertations. 1246. https://corescholar.libraries.wright.edu/etd_all/1246 This Dissertation is brought to you for free and open access by the Theses and Dissertations at CORE Scholar. It has been accepted for inclusion in Browse all Theses and Dissertations by an authorized administrator of CORE Scholar. For more information, please contact [email protected]. RAB3A AS A MODULATOR OF HOMEOSTATIC SYNAPTIC PLASTICITY A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy By ANDREW G. KOESTERS B.A., Miami University, 2004 2014 Wright State University WRIGHT STATE UNIVERSITY GRADUATE SCHOOL August 22, 2014 I HEREBY RECOMMEND THAT THE DISSERTATION PREPARED UNDER MY SUPERVISION BY Andrew G. Koesters ENTITLED Rab3A as a Modulator of Homeostatic Synaptic Plasticity BE ACCEPTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF Doctor of Philosophy. Kathrin Engisch, Ph.D. Dissertation Director Mill W. Miller, Ph.D. Director, Biomedical Sciences Ph.D. Program Committee on Final Examination Robert E. W. Fyffe, Ph.D. Vice President for Research Dean of the Graduate School Mark Rich, M.D./Ph.D. David Ladle, Ph.D. F. Javier Alvarez-Leefmans, M.D./Ph.D. Lynn Hartzler, Ph.D.
    [Show full text]
  • Disruption of NMDA Receptor Function Prevents Normal Experience
    Research Articles: Development/Plasticity/Repair Disruption of NMDA receptor function prevents normal experience-dependent homeostatic synaptic plasticity in mouse primary visual cortex https://doi.org/10.1523/JNEUROSCI.2117-18.2019 Cite as: J. Neurosci 2019; 10.1523/JNEUROSCI.2117-18.2019 Received: 16 August 2018 Revised: 7 August 2019 Accepted: 8 August 2019 This Early Release article has been peer-reviewed and accepted, but has not been through the composition and copyediting processes. The final version may differ slightly in style or formatting and will contain links to any extended data. Alerts: Sign up at www.jneurosci.org/alerts to receive customized email alerts when the fully formatted version of this article is published. Copyright © 2019 the authors Rodriguez et al. 1 Disruption of NMDA receptor function prevents normal experience-dependent homeostatic 2 synaptic plasticity in mouse primary visual cortex 3 4 Gabriela Rodriguez1,4, Lukas Mesik2,3, Ming Gao2,5, Samuel Parkins1, Rinki Saha2,6, 5 and Hey-Kyoung Lee1,2,3 6 7 8 1. Cell Molecular Developmental Biology and Biophysics (CMDB) Graduate Program, 9 Johns Hopkins University, Baltimore, MD 21218 10 2. Department of Neuroscience, Mind/Brain Institute, Johns Hopkins University, Baltimore, 11 MD 21218 12 3. Kavli Neuroscience Discovery Institute, Johns Hopkins University, Baltimore, MD 13 21218 14 4. Current address: Max Planck Florida Institute for Neuroscience, Jupiter, FL 33458 15 5. Current address: Division of Neurology, Barrow Neurological Institute, Pheonix, AZ 16 85013 17 6. Current address: Department of Psychiatry, Columbia University, New York, NY10032 18 19 Abbreviated title: NMDARs in homeostatic synaptic plasticity of V1 20 21 Corresponding Author: Hey-Kyoung Lee, Ph.D.
    [Show full text]
  • Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function
    Downloaded from http://cshperspectives.cshlp.org/ on September 25, 2021 - Published by Cold Spring Harbor Laboratory Press Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function Gina Turrigiano Department of Biology and Center for Behavioral Genomics, Brandeis University, Waltham, Massachusetts 02493 Correspondence: [email protected] Neural circuits must maintain stable function in the face of many plastic challenges, includ- ing changes in synapse number and strength, during learning and development. Recent work has shown that these destabilizing influences are counterbalanced by homeostatic plasticity mechanisms that act to stabilize neuronal and circuit activity. One such mechanism is syn- aptic scaling, which allows neurons to detect changes in their own firing rates through a set of calcium-dependent sensors that then regulate receptor trafficking to increase or decrease the accumulation of glutamate receptors at synaptic sites. Additional homeostatic mechanisms may allow local changes in synaptic activation to generate local synaptic adaptations, and network-wide changes in activity to generate network-wide adjustments in the balance between excitation and inhibition. The signaling pathways underlying these various forms of homeostatic plasticity are currently under intense scrutiny, and although dozens of mol- ecular pathways have now been implicated in homeostatic plasticity, a clear picture of how homeostatic feedback is structured at the molecular level has not yet emerged. On a functional level, neuronal networks likely use this complex set of regulatory mechanisms to achieve homeostasis over a wide range of temporal and spatial scales. ore than 50 years ago, Walter Cannon eter that is subject to homeostatic regulation. Mmarveled that “somehow the unstable During development billions of neurons wire stuff of which we are composed has learned themselves up into complex networks and man- the trick of maintaining stability” (Cannon age to reach a state where they can generate— 1932).
    [Show full text]
  • Tumor Necrosis Factor (TNF)-Receptor 1 and 2 Mediate Homeostatic Synaptic Plasticity of Denervated Mouse Dentate Granule Cells
    www.nature.com/scientificreports OPEN Tumor necrosis factor (TNF)- receptor 1 and 2 mediate homeostatic synaptic plasticity of Received: 04 March 2015 Accepted: 06 July 2015 denervated mouse dentate granule Published: 06 August 2015 cells Denise Becker†, Thomas Deller & Andreas Vlachos Neurological diseases are often accompanied by neuronal cell death and subsequent deafferentation of connected brain regions. To study functional changes after denervation we generated entorhino- hippocampal slice cultures, transected the entorhinal pathway, and denervated dentate granule cells in vitro. Our previous work revealed that partially denervated neurons respond to the loss of input with a compensatory, i.e., homeostatic, increase in their excitatory synaptic strength. TNFα maintains this denervation-induced homeostatic strengthening of excitatory synapses. Here, we used pharmacological approaches and mouse genetics to assess the role of TNF-receptor 1 and 2 in lesion-induced excitatory synaptic strengthening. Our experiments disclose that both TNF-receptors are involved in the regulation of denervation-induced synaptic plasticity. In line with this result TNF-receptor 1 and 2 mRNA-levels were upregulated after deafferentation in vitro. These findings implicate TNF-receptor signaling cascades in the regulation of homeostatic plasticity of denervated networks and suggest an important role for TNFα-signaling in the course of neurological diseases accompanied by deafferentation. Homeostatic control of cortical excitability, connectivity and plasticity is considered essential for normal brain function1–3. Work from the past years has unraveled a wealth of information on compensatory mechanisms acting in the brain to keep the activity in neuronal networks within a physiological range4. Among the best studied mechanisms is homeostatic synaptic plasticity5–8, which adjusts synaptic strength to changes in network activity in a compensatory manner.
    [Show full text]
  • Plasticity of Afferent-Specific Synapses in the Nucleus Accumbens By
    Plasticity of afferent-specific synapses in the nucleus accumbens By Brandon D. Turner Dissertation Submitted to the Faculty of the Graduate School of Vanderbilt University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY in Neuroscience August 10, 2018 Nashville, Tennessee Approved: Sachin Patel, M.D., Ph.D. Brad A. Grueter, Ph. D. Roger J. Colbran, Ph. D. Ralph J. DiLeone, Ph. D. This thesis is dedicated to my mother, father, brother, and friends who have stood by me through this long journey. And to my late grandfather, Robert Hope, for always pushing me one step further. ii ACKNOWLEGEMENTS This work would not have been possible without the members of the Grueter lab, current and former. I would like to especially thank Dr. Brad Grueter and Dr. Carrie Grueter and my thesis committee for their unwavering support and mentorship. iii TABLE OF CONTENTS Page DEDICATIONS ........................................................................................................................... ii ACKNOWLEDGEMENTS ........................................................................................................ iii LIST OF TABLES ...................................................................................................................... vi LIST OF FIGURES .................................................................................................................... vii Chapter 1. An introduction to motivation: The nucleus accumbens as the brain’s reward center .......... 1 2. Synaptic transmission
    [Show full text]
  • 1.32 Neural Computation Theories of Learning
    1.32 Neural Computation Theories of Learningq Samat Moldakarimov and Terrence J Sejnowski, University of California – San Diego, La Jolla, CA, United States; and Salk Institute for Biological Studies, La Jolla, CA, United States Ó 2017 Elsevier Ltd. All rights reserved. 1.32.1 Introduction 579 1.32.2 Hebbian Learning 580 1.32.3 Unsupervised Learning 581 1.32.4 Supervised Learning 581 1.32.5 Reinforcement Learning 583 1.32.6 Spike Timing–Dependent Plasticity 584 1.32.7 Plasticity of Intrinsic Excitability 586 1.32.8 Homeostatic Plasticity 586 1.32.9 Complexity of Learning 587 1.32.10 Conclusions 588 References 588 1.32.1 Introduction The anatomical discoveries in the 19th century and the physiological studies in the 20th century showed that the brain was made of networks of neurons connected together through synapses (Kandel et al., 2012). These discoveries led to a theory that learning could be the consequence of changes in the strengths of the synapses (Hebb, 1949). The Hebb’s rule for synaptic plasticity states that: When an axon of cell A is near enough to excite cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’sefficiency, as one of the cells firing B, is increased. Hebb (1949). This postulate was experimentally confirmed in the hippocampus, where high-frequency stimulation (HFS) of a presynaptic neuron causes long-term potentiation (LTP) in the synapses connecting it to the postsynaptic neurons (Bliss and Lomo, 1973). LTP takes place only if the postsynaptic cell is also active and sufficiently depolarized (Kelso et al., 1986).
    [Show full text]
  • Rapid Homeostatic Plasticity of Intrinsic Excitability in a Central Pattern Generator Network Stabilizes Functional Neural Network Output
    The Journal of Neuroscience, July 11, 2012 • 32(28):9649–9658 • 9649 Cellular/Molecular Rapid Homeostatic Plasticity of Intrinsic Excitability in a Central Pattern Generator Network Stabilizes Functional Neural Network Output Joseph L. Ransdell,1 Satish S. Nair,2 and David J. Schulz1 1Division of Biological Sciences and 2Department of Electrical and Computer Engineering, University of Missouri-Columbia, Columbia, Missouri 65211 Neurons and networks undergo a process of homeostatic plasticity that stabilizes output by integrating activity levels with network and cellular properties to counter longer-term perturbations. Here we describe a rapid compensatory interaction among a pair of potassium currents, IA and IKCa , that stabilizes both intrinsic excitability and network function in the cardiac ganglion of the crab, Cancer borealis. We determined that mRNA levels in single identified neurons for the channels which encode IA and IKCa are positively correlated, yet the ionic currents themselves are negatively correlated, across a population of motor neurons. We then determined that these currents are functionally coupled; decreasing levels of either current within a neuron causes a rapid increase in the other. This functional interdepen- dence results in homeostatic stabilization of both the individual neuronal and the network output. Furthermore, these compensatory increases are mechanistically independent, suggesting robustness in the maintenance of neural network output that is critical for survival. Together, we generate a complete model for homeostatic plasticity from mRNA to network output where rapid post- translational compensatory mechanisms acting on a reservoir of channels proteins regulated at the level of gene expression provide homeostatic stabilization of both cellular and network activity. Introduction of changes in conductances in the crustacean stomatogastric gan- glion (STG) (Thoby-Brisson and Simmers, 1998, 2002).
    [Show full text]
  • Coordinated Regulation of CB1 Cannabinoid Receptors and Anandamide Metabolism
    bioRxiv preprint doi: https://doi.org/10.1101/2021.05.21.445170; this version posted May 23, 2021. 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. Coordinated regulation of CB1 cannabinoid receptors and anandamide metabolism stabilize network activity during homeostatic scaling down Abbreviated title: Endocannabinoids and Homeostatic Scaling-Down Michael Ye1, Sarah K. Monroe1, Sean M. Gay2, Michael L. Armstrong3, Diane E. Youngstrom1, Fabio L. Urbina1, Stephanie L. Gupton1,2, Nichole Reisdorph3, Graham H Diering1,2,4* Affiliations 1. Department of Cell Biology and Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA 27599 2. UNC Neuroscience Center 3. Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO, USA 80045 4. Carolina Institute for Developmental Disabilities *Correspondence: [email protected] Number of pages: 36 Number of figures: 6 Number of words: abstract (241), introduction (643), discussion (1483) Conflict of interest: The authors declare no competing financial interests Acknowledgements: This work was supported by a grant to GHD from the National Institutes of Health (RF1AG068063), and to SLG (R01NS112326). 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.05.21.445170; this version posted May 23, 2021. 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 Neurons express overlapping homeostatic mechanisms to regulate synaptic function and network properties in response to perturbations of neuronal activity. Endocannabinoids (eCBs) are bioactive lipids synthesized in the post-synaptic compartments that regulate synaptic transmission, plasticity, and neuronal excitability throughout much of the brain, by activating pre- synaptic cannabinoid receptor CB1.
    [Show full text]
  • Integrating Hebbian and Homeostatic Plasticity: the Current State of the Field and Future Research Directions
    Integrating Hebbian and homeostatic plasticity: the current state of the field and future research directions Co-authors: 1 2 3 4 5 Tara Keck *, Taro Toyoizumi *, Lu Chen , Brent Doiron , Daniel E. Feldman , Kevin 6 7 8 9 10 Fox , Wulfram Gerstner , Philip G. Haydon , Mark Hübener , Hey-Kyoung Lee , 11 9 l6 12 John E. Lisman , Tobias Rose , Frank Sengpiel , David Stellwagen , Michael P. 13 11 14 Stryker , Gina G. Turrigiano , Mark C. van Rossum Affiliations 1. Department of Neuroscience, Physiology and Pharmacology, University College London, UK 2. RIKEN Brain Sciences Institute, Japan 3. Department of Neurosurgery, Stanford University, USA 4. Department of Mathematics, University of Pittsburgh, USA 5. Department of Molecular and Cell Biology, University of California, Berkeley, USA 6. Division of Neuroscience, University of Cardiff, UK 7. Brain Mind Institute, École Polytechnique Fédérale de Lausanne, Switzerland 8. Tufts University School of Medicine, USA 9. Department of Cellular and Systems Neuroscience, Max Planck Institute of Neurobiology, Germany 10. The Zanvyl Krieger Mind/Brain Institute, Johns Hopkins University, USA 11. Department of Biology, Brandeis University, USA 12. Centre for Research in Neuroscience, McGill University, Canada 13. Sandler Neurosciences Center, University of California, San Francisco, USA 14. School of Informatics, University of Edinburgh, UK *These authors contributed equally to this work We summarize here the results presented and subsequent discussion from the meeting on Integrating Hebbian and Homeostatic Plasticity at the Royal Society in April 2016. We first outline the major themes and results presented at the meeting. We next provide a synopsis of the outstanding questions that emerged from the discussion at the end of the meeting and finally suggest potential directions of research that we believe are most promising to develop an understanding of how these two forms of plasticity interact to facilitate functional changes in the brain.
    [Show full text]
  • Synaptic Up-Scaling Preserves Motor Circuit Output After Chronic, Natural Inactivity Joseph M Santin1,2*, Mauricio Vallejo2, Lynn K Hartzler2
    RESEARCH ARTICLE Synaptic up-scaling preserves motor circuit output after chronic, natural inactivity Joseph M Santin1,2*, Mauricio Vallejo2, Lynn K Hartzler2 1Division of Biological Sciences, University of Missouri-Columbia, Columbia, United States; 2Department of Biological Sciences, Wright State University, Dayton, United States Abstract Neural systems use homeostatic plasticity to maintain normal brain functions and to prevent abnormal activity. Surprisingly, homeostatic mechanisms that regulate circuit output have mainly been demonstrated during artificial and/or pathological perturbations. Natural, physiological scenarios that activate these stabilizing mechanisms in neural networks of mature animals remain elusive. To establish the extent to which a naturally inactive circuit engages mechanisms of homeostatic plasticity, we utilized the respiratory motor circuit in bullfrogs that normally remains inactive for several months during the winter. We found that inactive respiratory motoneurons exhibit a classic form of homeostatic plasticity, up-scaling of AMPA-glutamate receptors. Up-scaling increased the synaptic strength of respiratory motoneurons and acted to boost motor amplitude from the respiratory network following months of inactivity. Our results show that synaptic scaling sustains strength of the respiratory motor output following months of inactivity, thereby supporting a major neuroscience hypothesis in a normal context for an adult animal. DOI: https://doi.org/10.7554/eLife.30005.001 *For correspondence: Introduction [email protected] For the brain to work properly, neurons must employ compensatory mechanisms to retain informa- tion in synapses and to maintain normal circuit function. These compensatory mechanisms are con- Competing interests: The sidered homeostatic if they regulate firing frequency and/or circuit activity around a set-point, but authors declare that no they also may oppose disturbances to neuronal function without being firmly homeostatic (Turri- competing interests exist.
    [Show full text]
  • Mirna-Dependent Control of Homeostatic Plasticity in Neurons Sandra Dubes, Alexandre Favereaux, Olivier Thoumine, Mathieu Letellier
    miRNA-Dependent Control of Homeostatic Plasticity in Neurons Sandra Dubes, Alexandre Favereaux, Olivier Thoumine, Mathieu Letellier To cite this version: Sandra Dubes, Alexandre Favereaux, Olivier Thoumine, Mathieu Letellier. miRNA-Dependent Con- trol of Homeostatic Plasticity in Neurons. Frontiers in Cellular Neuroscience, Frontiers, 2019, 13, 10.3389/fncel.2019.00536. hal-02403037 HAL Id: hal-02403037 https://hal.archives-ouvertes.fr/hal-02403037 Submitted on 24 Nov 2020 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. fncel-13-00536 December 3, 2019 Time: 17:28 # 1 MINI REVIEW published: 05 December 2019 doi: 10.3389/fncel.2019.00536 miRNA-Dependent Control of Homeostatic Plasticity in Neurons Sandra Dubes1,2, Alexandre Favereaux1,2, Olivier Thoumine1,2 and Mathieu Letellier1,2* 1 University of Bordeaux, Interdisciplinary Institute for Neuroscience, UMR 5297, Bordeaux, France, 2 CNRS, Interdisciplinary Institute for Neuroscience, UMR 5297, Bordeaux, France Homeostatic plasticity is a form of plasticity in which neurons compensate for changes in neuronal activity through the control of key physiological parameters such as the number and the strength of their synaptic inputs and intrinsic excitability. Recent studies revealed that miRNAs, which are small non-coding RNAs repressing mRNA translation, participate in this process by controlling the translation of multiple effectors such as glutamate transporters, receptors, signaling molecules and voltage-gated ion Edited by: channels.
    [Show full text]
  • Homeostatic Regulation of Long-Term Potentiation
    Homeostatic regulation of long-term potentiation Dissertation zur Erlangung des Grades eines Doktors der Naturwissenschaften der Fakultät für Biologie der Ludwigs-Maximilians-Universität München Vorgelegt von Claudia Roth-Alpermann München, im Januar 2005 Ehrenwörtliche Versicherung Ich versichere hiermit ehrenwörtlich, dass die vorgelegte Dissertation von mir selbständig und ohne unerlaubte Beihilfe angefertigt ist. Claudia Roth-Alpermann München, den 23. Januar 2005 Tag der mündlichen Prüfung: 23. Februar 2005 Prüfungskommission: Prof. Dr. Tobias Bonhoeffer Prof. Dr. Martin Korte Prof. Dr. Benedikt Grothe Prof. Dr. Rainer Uhl Acknowledgements I would like to thank Professor Tobias Bonhoeffer for initiating this project, together with Profes- sor Richard Morris, and for giving me the opportunity to perform the experiments in his laborato- ry. I am grateful that I could work in an atmosphere of freedom and personal responsibility. Yet, he gave his scientific and personal advice whenever I asked for it. I was fortunate to have Professor Martin Korte as advisor. He taught me a lot – about science and beyond. He stirred questions, gave advice, and provided encouragement in the right dosage. I thank him for all the time and effort and for his guidance and friendship throughout the years. I am deeply indebted to Volker Staiger for his outstanding technical assistance. He helped me with countless smaller and bigger problems without ever losing his patience, and I appreciate his moral at least as high as his technical support. I wish to thank Professor Richard Morris for his continued and enthusiastic interest in this project. Exchanging ideas with him was a delightful source of inspiration. I would like to thank Professor Axel Borst for the knowledge and advice he extended to me – for- merly as my academic teacher at the University of Tübingen and now as member of my thesis commi�ee.
    [Show full text]