LTP, STP, and Scaling: Electrophysiological, Biochemical, and Structural Mechanisms
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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]. -
Ce Document Est Le Fruit D'un Long Travail Approuvé Par Le Jury De Soutenance Et Mis À Disposition De L'ensemble De La Communauté Universitaire Élargie
AVERTISSEMENT Ce document est le fruit d'un long travail approuvé par le jury de soutenance et mis à disposition de l'ensemble de la communauté universitaire élargie. Il est soumis à la propriété intellectuelle de l'auteur. Ceci implique une obligation de citation et de référencement lors de l’utilisation de ce document. D'autre part, toute contrefaçon, plagiat, reproduction illicite encourt une poursuite pénale. Contact : [email protected] LIENS Code de la Propriété Intellectuelle. articles L 122. 4 Code de la Propriété Intellectuelle. articles L 335.2- L 335.10 http://www.cfcopies.com/V2/leg/leg_droi.php http://www.culture.gouv.fr/culture/infos-pratiques/droits/protection.htm Ecole´ doctorale IAEM Lorraine D´epartement de formation doctorale en informatique Apprentissage spatial de corr´elations multimodales par des m´ecanismes d'inspiration corticale THESE` pour l'obtention du Doctorat de l'universit´ede Lorraine (sp´ecialit´einformatique) par Mathieu Lefort Composition du jury Pr´esident: Jean-Christophe Buisson, Professeur, ENSEEIHT Rapporteurs : Arnaud Revel, Professeur, Universit´ede La Rochelle Hugues Berry, CR HDR, INRIA Rh^one-Alpes Examinateurs : Beno^ıtGirard, CR HDR, CNRS ISIR Yann Boniface, MCF, Universit´ede Lorraine Directeur de th`ese: Bernard Girau, Professeur, Universit´ede Lorraine Laboratoire Lorrain de Recherche en Informatique et ses Applications | UMR 7503 Mis en page avec la classe thloria. i À tous ceux qui ont trouvé ou trouveront un intérêt à lire ce manuscrit ou à me côtoyer. ii iii Remerciements Je tiens à remercier l’ensemble de mes rapporteurs, Arnaud Revel et Hugues Berry, pour avoir accepter de prendre le temps d’évaluer mon travail et de l’avoir commenté de manière constructive malgré les délais relativement serrés. -
Diminished Neuronal Activity Increases Neuron–Neuron Connectivity Underlying Silent Synapse Formation and the Rapid Conversion of Silent to Functional Synapses
4040 • The Journal of Neuroscience, April 20, 2005 • 25(16):4040–4051 Cellular/Molecular Diminished Neuronal Activity Increases Neuron–Neuron Connectivity Underlying Silent Synapse Formation and the Rapid Conversion of Silent to Functional Synapses Kimiko Nakayama, Kazuyuki Kiyosue, and Takahisa Taguchi Neuronics Research Group, Research Institute for Cell Engineering, National Institute of Advanced Industrial Science and Technology, Ikeda, Osaka 563- 8577, Japan Neuronal activity regulates the synaptic strength of neuronal networks. However, it is still unclear how diminished activity changes connection patterns in neuronal circuits. To address this issue, we analyzed neuronal connectivity and relevant mechanisms using hippocampal cultures in which developmental synaptogenesis had occurred. We show that diminution of network activity in mature neuronal circuit promotes reorganization of neuronal circuits via NR2B subunit-containing NMDA-type glutamate receptors (NR2B- NMDARs), which mediate silent synapse formation. Simultaneous double whole-cell recordings revealed that diminishing neuronal circuit activity for 48 h increased the number of synaptically connected neuron pairs with both silent and functional synapses. This increase was accompanied by the specific expression of NR2B-NMDARs at synaptic sites. Analysis of miniature EPSCs (mEPSCs) showed that the frequency of NMDAR-mediated, but not AMPAR-mediated, mEPSCs increased, indicating that diminished neuronal activity promotes silent synapse formation via the surface delivering NR2B-NMDARs in mature neurons. After activation of neuronal circuit by releasing from TTX blockade (referred as circuit reactivation), the frequency of AMPAR-mediated mEPSCs increased instead, and this increase was prevented by ifenprodil. The circuit reactivation also caused an increased colocalization of glutamate receptor 1-specfic and synaptic NR2B-specific puncta. -
Gut Microbiota and Neuroplasticity
cells Review Gut Microbiota and Neuroplasticity Julia Murciano-Brea 1,2, Martin Garcia-Montes 1,2, Stefano Geuna 3 and Celia Herrera-Rincon 1,2,* 1 Department of Biodiversity, Ecology & Evolution, Biomathematics Unit, Complutense University of Madrid, 28040 Madrid, Spain; [email protected] (J.M.-B.); [email protected] (M.G.-M.) 2 Modeling, Data Analysis and Computational Tools for Biology Research Group, Complutense University of Madrid, 28040 Madrid, Spain 3 Department of Clinical and Biological Sciences, School of Medicine, University of Torino, 10124 Torino, Italy; [email protected] * Correspondence: [email protected]; Tel.: +34-91394-4888 Abstract: The accumulating evidence linking bacteria in the gut and neurons in the brain (the microbiota–gut–brain axis) has led to a paradigm shift in the neurosciences. Understanding the neurobiological mechanisms supporting the relevance of actions mediated by the gut microbiota for brain physiology and neuronal functioning is a key research area. In this review, we discuss the literature showing how the microbiota is emerging as a key regulator of the brain’s function and behavior, as increasing amounts of evidence on the importance of the bidirectional communication between the intestinal bacteria and the brain have accumulated. Based on recent discoveries, we suggest that the interaction between diet and the gut microbiota, which might ultimately affect the brain, represents an unprecedented stimulus for conducting new research that links food and mood. We also review the limited work in the clinical arena to date, and we propose novel approaches for deciphering the gut microbiota–brain axis and, eventually, for manipulating this relationship to boost mental wellness. -
A Review of Glutamate Receptors I: Current Understanding of Their Biology
J Toxicol Pathol 2008; 21: 25–51 Review A Review of Glutamate Receptors I: Current Understanding of Their Biology Colin G. Rousseaux1 1Department of Pathology and Laboratory Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada Abstract: Seventy years ago it was discovered that glutamate is abundant in the brain and that it plays a central role in brain metabolism. However, it took the scientific community a long time to realize that glutamate also acts as a neurotransmitter. Glutamate is an amino acid and brain tissue contains as much as 5 – 15 mM glutamate per kg depending on the region, which is more than of any other amino acid. The main motivation for the ongoing research on glutamate is due to the role of glutamate in the signal transduction in the nervous systems of apparently all complex living organisms, including man. Glutamate is considered to be the major mediator of excitatory signals in the mammalian central nervous system and is involved in most aspects of normal brain function including cognition, memory and learning. In this review, the basic biology of the excitatory amino acids glutamate, glutamate receptors, GABA, and glycine will first be explored. In the second part of this review, the known pathophysiology and pathology will be described. (J Toxicol Pathol 2008; 21: 25–51) Key words: glutamate, glycine, GABA, glutamate receptors, ionotropic, metabotropic, NMDA, AMPA, review Introduction and Overview glycine), peptides (vasopressin, somatostatin, neurotensin, etc.), and monoamines (norepinephrine, dopamine and In the first decades of the 20th century, research into the serotonin) plus acetylcholine. chemical mediation of the “autonomous” (autonomic) Glutamatergic synaptic transmission in the mammalian nervous system (ANS) was an area that received much central nervous system (CNS) was slowly established over a research activity. -
Metaplasticity of Mossy Fiber Synaptic Transmission Involves Altered Release Probability
The Journal of Neuroscience, May 1, 2000, 20(9):3434–3441 Metaplasticity of Mossy Fiber Synaptic Transmission Involves Altered Release Probability Ivan V. Goussakov,1 Klaus Fink,2 Christian E. Elger,1 and Heinz Beck1 1Department of Epileptology, University of Bonn, 53105 Bonn, Germany, and 2Department of Pharmacology, University of Bonn, 53113 Bonn, Germany Activity-dependent synaptic plasticity is a fundamental feature but not in kainate-treated animals, indicating that status- of CNS synapses. Intriguingly, the capacity of synapses to induced changes occur downstream of protein kinase A. To test express plastic changes is itself subject to considerable whether altered neurotransmitter release might account for activity-dependent variation, or metaplasticity. These forms of these changes, we measured the size of the releasable pool of higher order plasticity are important because they may be glutamate in mossy fiber terminals. We find that the size of the crucial to maintain synapses within a dynamic functional range. releasable pool of glutamate was significantly increased in In this study, we asked whether neuronal activity induced in vivo kainate-treated rats, indicating an increased release probability by application of kainate can induce lasting changes in mossy at the mossy fiber-CA3 synapse. fiber short- and long-term plasticity. Therefore, we suggest that lasting changes in neurotransmit- Several weeks after kainate-induced status epilepticus, the ter release probability caused by neuronal activity may be a mossy fiber, but not the associational-commissural pathway, powerful mechanism for metaplasticity that modulates both exhibits a marked loss of paired-pulse facilitation, augmenta- short- and long-term plasticity in the mossy fiber-CA3 synapse tion, and long-term potentiation (LTP). -
Unconventional NMDA Receptor Signaling
10800 • The Journal of Neuroscience, November 8, 2017 • 37(45):10800–10807 Symposium Unconventional NMDA Receptor Signaling X Kim Dore,1 Ivar S. Stein,2 XJennifer A. Brock,3,4 XPablo E. Castillo,5 XKaren Zito,2 and XP. Jesper Sjo¨stro¨m4 1Department of Neuroscience and Section for Neurobiology, Division of Biology, Center for Neural Circuits and Behavior, University of California, San Diego, California 92093, 2Center for Neuroscience, University of California, Davis, California 95618, 3Integrated Program in Neuroscience, McGill University, Montreal, Quebec H3A 2B4, Canada, 4Centre for Research in Neuroscience, Brain Repair and Integrative Neuroscience Programme, Department of Neurology and Neurosurgery, Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec H3G 1A4, Canada, and 5Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461 In the classical view, NMDA receptors (NMDARs) are stably expressed at the postsynaptic membrane, where they act via Ca 2ϩ to signal coincidence detection in Hebbian plasticity. More recently, it has been established that NMDAR-mediated transmission can be dynam- ically regulated by neural activity. In addition, NMDARs have been found presynaptically, where they cannot act as conventional coin- cidence detectors. Unexpectedly, NMDARs have also been shown to signal metabotropically, without the need for Ca 2ϩ. This review highlights novel findings concerning these unconventional modes of NMDAR action. Key words: -
Enhancing Nervous System Recovery Through Neurobiologics, Neural Interface Training, and Neurorehabilitation
UCLA UCLA Previously Published Works Title Enhancing Nervous System Recovery through Neurobiologics, Neural Interface Training, and Neurorehabilitation. Permalink https://escholarship.org/uc/item/0rb4m424 Authors Krucoff, Max O Rahimpour, Shervin Slutzky, Marc W et al. Publication Date 2016 DOI 10.3389/fnins.2016.00584 Peer reviewed eScholarship.org Powered by the California Digital Library University of California REVIEW published: 27 December 2016 doi: 10.3389/fnins.2016.00584 Enhancing Nervous System Recovery through Neurobiologics, Neural Interface Training, and Neurorehabilitation Max O. Krucoff 1*, Shervin Rahimpour 1, Marc W. Slutzky 2, 3, V. Reggie Edgerton 4 and Dennis A. Turner 1, 5, 6 1 Department of Neurosurgery, Duke University Medical Center, Durham, NC, USA, 2 Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA, 3 Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA, 4 Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA, 5 Department of Neurobiology, Duke University Medical Center, Durham, NC, USA, 6 Research and Surgery Services, Durham Veterans Affairs Medical Center, Durham, NC, USA After an initial period of recovery, human neurological injury has long been thought to be static. In order to improve quality of life for those suffering from stroke, spinal cord injury, or traumatic brain injury, researchers have been working to restore the nervous system and reduce neurological deficits through a number of mechanisms. For example, Edited by: neurobiologists have been identifying and manipulating components of the intra- and Ioan Opris, University of Miami, USA extracellular milieu to alter the regenerative potential of neurons, neuro-engineers have Reviewed by: been producing brain-machine and neural interfaces that circumvent lesions to restore Yoshio Sakurai, functionality, and neurorehabilitation experts have been developing new ways to revitalize Doshisha University, Japan Brian R. -
Activity-Dependent Metaplasticity of Inhibitory and Excitatory Synaptic Transmission in the Lamprey Spinal Cord Locomotor Network
The Journal of Neuroscience, March 1, 1999, 19(5):1647–1656 Activity-Dependent Metaplasticity of Inhibitory and Excitatory Synaptic Transmission in the Lamprey Spinal Cord Locomotor Network David Parker and Sten Grillner Nobel Institute for Neurophysiology, Department of Neuroscience, Karolinska Institute, S-17177, Stockholm, Sweden Paired intracellular recordings have been used to examine the activity-dependent plasticity will presumably not contribute to activity-dependent plasticity and neuromodulator-induced the patterning of network activity. However, in the presence of metaplasticity of synaptic inputs from identified inhibitory and the neuromodulators substance P and 5-HT, significant activity- excitatory interneurons in the lamprey spinal cord. Trains of dependent metaplasticity of these inputs developed over the spikes at 5–20 Hz were used to mimic the frequency of spiking first five spikes in the train. Substance P induced significant that occurs in network interneurons during NMDA or brainstem- activity-dependent depression of inhibitory but potentiation of evoked locomotor activity. Inputs from inhibitory and excitatory excitatory interneuron inputs, whereas 5-HT induced significant interneurons exhibited similar activity-dependent changes, with activity-dependent potentiation of both inhibitory and excita- synaptic depression developing during the spike train. The level tory interneuron inputs. Because these metaplastic effects are of depression reached was greater with lower stimulation fre- consistent with the substance P and 5-HT-induced modulation quencies. Significant activity-dependent depression of inputs of the network output, activity-dependent metaplasticity could from excitatory interneurons and inhibitory crossed caudal in- be a potential mechanism underlying the coordination and terneurons, which are central elements in the patterning of modulation of rhythmic network activity. -
A Synthetic Likelihood Solution to the Silent Synapse Estimation Problem
bioRxiv preprint doi: https://doi.org/10.1101/781898; this version posted September 25, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Classification: Biological sciences (Neuroscience) Title: A synthetic likelihood solution to the silent synapse estimation problem Authors: Michael Lynna, Kevin F.H. Leea, Cary Soaresa, Richard Nauda,e & Jean-Claude Béïquea,b,c,d Affiliations: a Department of Cellular and Molecular Medicine, bCanadian Partnership for Stroke Recovery, c Centre for Neural Dynamics, d Brain and Mind Research Institute, University of Ottawa, Ottawa, Canada K1H 8M5 eDepartment of Physics, STEM Complex, room 336, 150 Louis Pasteur Pvt., University of Ottawa, K1N 6N5, Ottawa, Canada. Corresponding author: Jean-Claude Beique University of Ottawa 451 Smyth Road, RGN 3501N Ottawa, Ontario, Canada K1H 8M5 Tel: 1-613-562-5800 ext. 4968 [email protected] Keywords: silent synapses, plasticity, statistical inference, synthetic likelihood bioRxiv preprint doi: https://doi.org/10.1101/781898; this version posted September 25, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Abstract The proportions of AMPA-lacking silent synapses are believed to play a fundamental role in determining the plasticity potential of neural networks. It is, however, unclear whether current methods to quantify silent synapses possess adequate estimation properties. -
Conceptual Nervous System”: Can Computational Cognitive Neuroscience Transform Learning Theory?
Beyond the “Conceptual Nervous System”: Can Computational Cognitive Neuroscience Transform Learning Theory? Fabian A. Sotoa,∗ aDepartment of Psychology, Florida International University, 11200 SW 8th St, AHC4 460, Miami, FL 33199 Abstract In the last century, learning theory has been dominated by an approach assuming that associations between hypothetical representational nodes can support the acquisition of knowledge about the environment. The similarities between this approach and connectionism did not go unnoticed to learning theorists, with many of them explicitly adopting a neural network approach in the modeling of learning phenomena. Skinner famously criticized such use of hypothetical neural structures for the explanation of behavior (the “Conceptual Nervous System”), and one aspect of his criticism has proven to be correct: theory underdetermination is a pervasive problem in cognitive modeling in general, and in associationist and connectionist models in particular. That is, models implementing two very different cognitive processes often make the exact same behavioral predictions, meaning that important theoretical questions posed by contrasting the two models remain unanswered. We show through several examples that theory underdetermination is common in the learning theory literature, affecting the solvability of some of the most important theoretical problems that have been posed in the last decades. Computational cognitive neuroscience (CCN) offers a solution to this problem, by including neurobiological constraints in computational models of behavior and cognition. Rather than simply being inspired by neural computation, CCN models are built to reflect as much as possible about the actual neural structures thought to underlie a particular behavior. They go beyond the “Conceptual Nervous System” and offer a true integration of behavioral and neural levels of analysis. -
Intracellular Domains of NMDA Receptor Subtypes Are Determinants for Long-Term Potentiation Induction
The Journal of Neuroscience, November 26, 2003 • 23(34):10791–10799 • 10791 Cellular/Molecular Intracellular Domains of NMDA Receptor Subtypes Are Determinants for Long-Term Potentiation Induction Georg Ko¨hr,1 Vidar Jensen,3 Helmut J. Koester,2 Andre L. A. Mihaljevic,1 Jo K. Utvik,4 Ane Kvello,3 Ole P. Ottersen,4 Peter H. Seeburg,1 Rolf Sprengel,1 and Øivind Hvalby3 1Max-Planck-Institute for Medical Research, D-69120 Heidelberg, Germany, 2Baylor College of Medicine, Houston, Texas 77030, and 3Institute of Basic Medical Sciences and 4Centre for Molecular Biology and Neuroscience and Department of Anatomy, University of Oslo, N-0317 Oslo, Norway NMDA receptors (NMDARs) are essential for modulating synaptic strength at central synapses. At hippocampal CA3-to-CA1 synapses of adult mice, different NMDAR subtypes with distinct functionality assemble from NR1 with NR2A and/or NR2B subunits. Here we investigated the role of these NMDA receptor subtypes in long-term potentiation (LTP) induction. Because of the higher NR2B contri- bution in the young hippocampus, LTP of extracellular field potentials could be enhanced by repeated tetanic stimulation in young but not in adult mice. Similarly, NR2B-specific antagonists reduced LTP in young but only marginally in adult wild-type mice, further demonstrating that in mature CA3-to-CA1 connections LTP induction results primarily from NR2A-type signaling. This finding is also supported by gene-targeted mutant mice expressing C-terminally truncated NR2A subunits, which participate in synaptic NMDAR ϩ channel formation and Ca 2 signaling, as indicated by immunopurified synaptic receptors, postembedding immunogold labeling, and ϩ spinous Ca 2 transients in the presence of NR2B blockers.