Synaptic and Nonsynaptic Plasticity Approximating Probabilistic Inference
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DIVERGENT SCALING of MINIATURE EXCITATORY POST-SYNAPTIC CURRENT AMPLITUDES in HOMEOSTATIC PLASTICITY a Dissertation Submitted In
DIVERGENT SCALING OF MINIATURE EXCITATORY POST-SYNAPTIC CURRENT AMPLITUDES IN HOMEOSTATIC PLASTICITY A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy by AMANDA L. HANES M.S., Wright State University, 2009 B.S.C.S., Wright State University, 2006 2018 Wright State University WRIGHT STATE UNIVERSITY GRADUATE SCHOOL December 12, 2018 I HEREBY RECOMMEND THAT THE DISSERTATION PREPARED UNDER MY SUPERVISION BY Amanda L. Hanes ENTITLED Divergent scaling of miniature post-synaptic current amplitudes in homeostatic plasticity BE ACCEPTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF Doctor of Philosophy. ________________________________ Kathrin L. Engisch, Ph.D Dissertation Director ________________________________ Mill W. Miller, Ph.D. Director, Biomedical Sciences PhD Program ________________________________ Barry Milligan, Ph.D. Interim Dean of the Graduate School Committee on Final Examination: ________________________________ Mark Rich, M.D./Ph.D. ________________________________ David Ladle, Ph.D. ________________________________ Michael Raymer, Ph.D. ________________________________ Courtney Sulentic, Ph.D. ABSTRACT Hanes, Amanda L. Ph.D. Biomedical Sciences PhD Program, Wright State University, 2018. Divergent scaling of miniature excitatory post-synaptic current amplitudes in homeostatic plasticity Synaptic plasticity, the ability of neurons to modulate their inputs in response to changing stimuli, occurs in two forms which have opposing effects on synaptic physiology. Hebbian plasticity induces rapid, persistent changes at individual synapses in a positive feedback manner. Homeostatic plasticity is a negative feedback effect that responds to chronic changes in network activity by inducing opposing, network-wide changes in synaptic strength and restoring activity to its original level. The changes in synaptic strength can be measured as changes in the amplitudes of miniature post- synaptic excitatory currents (mEPSCs). -
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. -
Electromagnetic Field and TGF-Β Enhance the Compensatory
www.nature.com/scientificreports OPEN Electromagnetic feld and TGF‑β enhance the compensatory plasticity after sensory nerve injury in cockroach Periplaneta americana Milena Jankowska1, Angelika Klimek1, Chiara Valsecchi2, Maria Stankiewicz1, Joanna Wyszkowska1* & Justyna Rogalska1 Recovery of function after sensory nerves injury involves compensatory plasticity, which can be observed in invertebrates. The aim of the study was the evaluation of compensatory plasticity in the cockroach (Periplaneta americana) nervous system after the sensory nerve injury and assessment of the efect of electromagnetic feld exposure (EMF, 50 Hz, 7 mT) and TGF‑β on this process. The bioelectrical activities of nerves (pre‑and post‑synaptic parts of the sensory path) were recorded under wind stimulation of the cerci before and after right cercus ablation and in insects exposed to EMF and treated with TGF‑β. Ablation of the right cercus caused an increase of activity of the left presynaptic part of the sensory path. Exposure to EMF and TGF‑β induced an increase of activity in both parts of the sensory path. This suggests strengthening efects of EMF and TGF‑β on the insect ability to recognize stimuli after one cercus ablation. Data from locomotor tests proved electrophysiological results. The takeover of the function of one cercus by the second one proves the existence of compensatory plasticity in the cockroach escape system, which makes it a good model for studying compensatory plasticity. We recommend further research on EMF as a useful factor in neurorehabilitation. Injuries in the nervous system caused by acute trauma, neurodegenerative diseases or even old age are hard to reverse and represent an enormous challenge for modern medicine. -
Spike-Based Bayesian-Hebbian Learning in Cortical and Subcortical Microcircuits
Spike-Based Bayesian-Hebbian Learning in Cortical and Subcortical Microcircuits PHILIP J. TULLY Doctoral Thesis Stockholm, Sweden 2017 TRITA-CSC-A-2017:11 ISSN 1653-5723 KTH School of Computer Science and Communication ISRN-KTH/CSC/A-17/11-SE SE-100 44 Stockholm ISBN 978-91-7729-351-4 SWEDEN Akademisk avhandling som med tillstånd av Kungl Tekniska högskolan framläg- ges till offentlig granskning för avläggande av teknologie doktorsexamen i datalogi tisdagen den 9 maj 2017 klockan 13.00 i F3, Lindstedtsvägen 26, Kungl Tekniska högskolan, Valhallavägen 79, Stockholm. © Philip J. Tully, May 2017 Tryck: Universitetsservice US AB iii Abstract Cortical and subcortical microcircuits are continuously modified throughout life. Despite ongoing changes these networks stubbornly maintain their functions, which persist although destabilizing synaptic and nonsynaptic mechanisms should osten- sibly propel them towards runaway excitation or quiescence. What dynamical phe- nomena exist to act together to balance such learning with information processing? What types of activity patterns do they underpin, and how do these patterns relate to our perceptual experiences? What enables learning and memory operations to occur despite such massive and constant neural reorganization? Progress towards answering many of these questions can be pursued through large- scale neuronal simulations. Inspiring some of the most seminal neuroscience exper- iments, theoretical models provide insights that demystify experimental measure- ments and even inform new experiments. In this thesis, a Hebbian learning rule for spiking neurons inspired by statistical inference is introduced. The spike-based version of the Bayesian Confidence Propagation Neural Network (BCPNN) learning rule involves changes in both synaptic strengths and intrinsic neuronal currents. -
New Clues for the Cerebellar Mechanisms of Learning
REVIEW Distributed Circuit Plasticity: New Clues for the Cerebellar Mechanisms of Learning Egidio D’Angelo1,2 & Lisa Mapelli1,3 & Claudia Casellato 5 & Jesus A. Garrido1,4 & Niceto Luque 4 & Jessica Monaco2 & Francesca Prestori1 & Alessandra Pedrocchi 5 & Eduardo Ros 4 Abstract The cerebellum is involved in learning and memory it can easily cope with multiple behaviors endowing therefore of sensory motor skills. However, the way this process takes the cerebellum with the properties needed to operate as an place in local microcircuits is still unclear. The initial proposal, effective generalized forward controller. casted into the Motor Learning Theory, suggested that learning had to occur at the parallel fiber–Purkinje cell synapse under Keywords Cerebellum . Distributed plasticity . Long-term supervision of climbing fibers. However, the uniqueness of this synaptic plasticity . LTP . LTD . Learning . Memory mechanism has been questioned, and multiple forms of long- term plasticity have been revealed at various locations in the cerebellar circuit, including synapses and neurons in the gran- Introduction ular layer, molecular layer and deep-cerebellar nuclei. At pres- ent, more than 15 forms of plasticity have been reported. There The cerebellum is involved in the acquisition of procedural mem- has been a long debate on which plasticity is more relevant to ory, and several attempts have been done at linking cerebellar specific aspects of learning, but this question turned out to be learning to the underlying neuronal circuit mechanisms. -
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. -
Control of Homeostatic Synaptic Plasticity by AKAP-Anchored Kinase and Phosphatase Regulation of Ca2+-Permeable AMPA Receptors
This Accepted Manuscript has not been copyedited and formatted. The final version may differ from this version. Research Articles: Cellular/Molecular Control of Homeostatic Synaptic Plasticity by AKAP-Anchored Kinase and Phosphatase Regulation of Ca2+-Permeable AMPA Receptors Jennifer L. Sanderson1, John D. Scott3,4 and Mark L. Dell'Acqua1,2 1Department of Pharmacology 2Program in Neuroscience, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO 80045, USA. 3Howard Hughes Medical Institute 4Department of Pharmacology, University of Washington School of Medicine, Seattle, WA 98195, USA. DOI: 10.1523/JNEUROSCI.2362-17.2018 Received: 21 August 2017 Revised: 17 January 2018 Accepted: 6 February 2018 Published: 13 February 2018 Author contributions: J.S., J.D.S., and M.L.D. designed research; J.S. performed research; J.S. and M.L.D. analyzed data; J.S., J.D.S., and M.L.D. wrote the paper; J.D.S. contributed unpublished reagents/analytic tools. Conflict of Interest: The authors declare no competing financial interests. This work was supported by NIH grant R01NS040701 (to M.L.D.). Contents are the authors' sole responsibility and do not necessarily represent official NIH views. The authors declare no competing financial interests. We thank Dr. Jason Aoto for critical reading of the manuscript. Corresponding author: Mark L. Dell'Acqua, Department of Pharmacology, University of Colorado School of Medicine, Mail Stop 8303, RC1-North, 12800 East 19th Ave Aurora, CO 80045. Email: [email protected] Cite as: J. Neurosci ; 10.1523/JNEUROSCI.2362-17.2018 Alerts: Sign up at www.jneurosci.org/cgi/alerts to receive customized email alerts when the fully formatted version of this article is published. -
Article Role of Delayed Nonsynaptic Neuronal Plasticity in Long-Term Associative Memory
Current Biology 16, 1269–1279, July 11, 2006 ª2006 Elsevier Ltd All rights reserved DOI 10.1016/j.cub.2006.05.049 Article Role of Delayed Nonsynaptic Neuronal Plasticity in Long-Term Associative Memory Ildiko´ Kemenes,1 Volko A. Straub,1,3 memory, and we describe how this information can be Eugeny S. Nikitin,1 Kevin Staras,1,4 Michael O’Shea,1 translated into modified network and behavioral output. Gyo¨ rgy Kemenes,1,2,* and Paul R. Benjamin1,2,* 1 Sussex Centre for Neuroscience Introduction Department of Biological and Environmental Sciences School of Life Sciences It is now widely accepted that nonsynaptic as well as University of Sussex synaptic plasticity are substrates for long-term memory Falmer, Brighton BN1 9QG [1–4]. Although information is available on how nonsy- United Kingdom naptic plasticity can emerge from cellular processes active during learning [3], far less is understood about how it is translated into persistently modified behavior. Summary There are, for instance, important unanswered ques- tions regarding the timing and persistence of nonsynap- Background: It is now well established that persistent tic plasticity and the relationship between nonsynaptic nonsynaptic neuronal plasticity occurs after learning plasticity and changes in synaptic output. In this paper and, like synaptic plasticity, it can be the substrate for we address these important issues by looking at an long-term memory. What still remains unclear, though, example of learning-induced nonsynaptic plasticity is how nonsynaptic plasticity contributes to the altered (somal depolarization), its onset and persistence, and neural network properties on which memory depends. its effects on synaptically mediated network activation Understanding how nonsynaptic plasticity is translated in an experimentally tractable molluscan model system. -
Modeling Prediction and Pattern Recognition in the Early Visual and Olfactory Systems
Modeling prediction and pattern recognition in the early visual and olfactory systems BERNHARD A. KAPLAN Doctoral Thesis Stockholm, Sweden 2015 TRITA-CSC-A-2015:10 ISSN-1653-5723 KTH School of Computer Science and Communication ISRN KTH/CSC/A-15/10-SE SE-100 44 Stockholm ISBN 978-91-7595-532-2 SWEDEN Akademisk avhandling som med tillstånd av Kungl Tekniska högskolan fram- lägges till offentlig granskning för avläggande av Doctoral Thesis in Computer Science onsdag 27:e maj 2015 klockan 10.00 i F3, Lindstedtsvägen 26, Kungl Tekniska högskolan, Stockholm. © Bernhard A. Kaplan, April 2015 Tryck: Universitetsservice US AB iii Abstract Our senses are our mind’s window to the outside world and deter- mine how we perceive our environment. Sensory systems are complex multi-level systems that have to solve a multitude of tasks that allow us to understand our surroundings. However, questions on various lev- els and scales remain to be answered ranging from low-level neural responses to behavioral functions on the highest level. Modeling can connect different scales and contribute towards tackling these questions by giving insights into perceptual processes and interactions between processing stages. In this thesis, numerical simulations of spiking neural networks are used to deal with two essential functions that sensory systems have to solve: pattern recognition and prediction. The focus of this thesis lies on the question as to how neural network connectivity can be used in order to achieve these crucial functions. The guiding ideas of the models presented here are grounded in the probabilistic interpretation of neural signals, Hebbian learning principles and connectionist ideas. -
The Interplay of Synaptic Plasticity and Scaling Enables Self-Organized
bioRxiv preprint doi: https://doi.org/10.1101/260950; this version posted August 27, 2018. 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 4.0 International license. Manuscript SUBMITTED TO eLife 1 The INTERPLAY OF SYNAPTIC PLASTICITY 2 AND SCALING ENABLES self-orGANIZED 3 FORMATION AND ALLOCATION OF MULTIPLE 4 MEMORY REPRESENTATIONS 1,2†§* 1,2† 1,2 5 Johannes Maria Auth , Timo Nachstedt , Christian TETZLAff *For CORRespondence: ThirD INSTITUTE OF Physics, Georg-August-Universität Göttingen, Germany; Bernstein [email protected] 6 1 2 (JMA) Center FOR Computational Neuroscience, Georg-August-Universität Göttingen, Germany 7 †These AUTHORS CONTRIBUTED EQUALLY TO THIS WORK 8 PrESENT ADDRess: §Department OF 9 NeurOBIOLOGY, The WEIZMANN AbstrACT IT IS COMMONLY ASSUMED THAT MEMORIES ABOUT EXPERIENCED STIMULI ARE REPRESENTED BY INSTITUTE OF Science, Rehovot, ISRAEL10 GROUPS OF HIGHLY INTERCONNECTED NEURONS CALLED CELL assemblies. This REQUIRES ALLOCATING AND STORING 11 INFORMATION IN THE NEURAL CIRCUITRY, WHICH HAPPENS THROUGH SYNAPTIC WEIGHT adaptation. IT Remains, 12 HOWEver, LARGELY UNKNOWN HOW MEMORY ALLOCATION AND STORAGE CAN BE ACHIEVED AND COORDINATED TO 13 ALLOW FOR A FAITHFUL REPRESENTATION OF MULTIPLE MEMORIES WITHOUT DISRUPTIVE INTERFERENCE BETWEEN 14 them. IN THIS THEORETICAL STUDY, WE SHOW THAT THE INTERPLAY BETWEEN CONVENTIONAL SYNAPTIC PLASTICITY 15 AND HOMEOSTATIC SYNAPTIC SCALING ORGANIZES SYNAPTIC WEIGHT ADAPTATIONS SUCH THAT A NEW STIMULUS 16 FORMS A NEW MEMORY AND WHERE DIffERENT STIMULI ARE ASSIGNED TO DISTINCT CELL assemblies. The 17 RESULTING DYNAMICS CAN REPRODUCE EXPERIMENTAL in-vivo data, FOCUSING ON HOW DIVERSE FACTORS AS 18 NEURONAL EXCITABILITY AND NETWORK CONNECTIVITY, INflUENCE MEMORY formation. -
Long-Term Plasticity of Intrinsic Excitability
Downloaded from learnmem.cshlp.org on September 27, 2021 - Published by Cold Spring Harbor Laboratory Press Review Long-Term Plasticity of Intrinsic Excitability: Learning Rules and Mechanisms Gae¨l Daoudal and Dominique Debanne1 Institut National de la Sante´Et de la Recherche Me´dicale UMR464 Neurobiologie des Canaux Ioniques, Institut Fe´de´ratif Jean Roche, Faculte´deMe´decine Secteur Nord, Universite´d’Aix-Marseille II, 13916 Marseille, France Spatio-temporal configurations of distributed activity in the brain is thought to contribute to the coding of neuronal information and synaptic contacts between nerve cells could play a central role in the formation of privileged pathways of activity. Synaptic plasticity is not the exclusive mode of regulation of information processing in the brain, and persistent regulations of ionic conductances in some specialized neuronal areas such as the dendrites, the cell body, and the axon could also modulate, in the long-term, the propagation of neuronal information. Persistent changes in intrinsic excitability have been reported in several brain areas in which activity is elevated during a classical conditioning. The role of synaptic activity seems to be a determinant in the induction, but the learning rules and the underlying mechanisms remain to be defined. We discuss here the role of synaptic activity in the induction of intrinsic plasticity in cortical, hippocampal, and cerebellar neurons. Activation of glutamate receptors initiates a long-term modification in neuronal excitability that may represent a parallel, synergistic substrate for learning and memory. Similar to synaptic plasticity, long-lasting intrinsic plasticity appears to be bidirectional and to express a certain level of input or cell specificity. -
Diverse Impact of Acute and Long-Term Extracellular Proteolytic Activity on Plasticity of Neuronal Excitability
REVIEW published: 10 August 2015 doi: 10.3389/fncel.2015.00313 Diverse impact of acute and long-term extracellular proteolytic activity on plasticity of neuronal excitability Tomasz Wójtowicz 1*, Patrycja Brzda, k 2 and Jerzy W. Mozrzymas 1,2 1 Laboratory of Neuroscience, Department of Biophysics, Wroclaw Medical University, Wroclaw, Poland, 2 Department of Animal Physiology, Institute of Experimental Biology, Wroclaw University, Wroclaw, Poland Learning and memory require alteration in number and strength of existing synaptic connections. Extracellular proteolysis within the synapses has been shown to play a pivotal role in synaptic plasticity by determining synapse structure, function, and number. Although synaptic plasticity of excitatory synapses is generally acknowledged to play a crucial role in formation of memory traces, some components of neural plasticity are reflected by nonsynaptic changes. Since information in neural networks is ultimately conveyed with action potentials, scaling of neuronal excitability could significantly enhance or dampen the outcome of dendritic integration, boost neuronal information storage capacity and ultimately learning. However, the underlying mechanism is poorly understood. With this regard, several lines of evidence and our most recent study support a view that activity of extracellular proteases might affect information processing Edited by: Leszek Kaczmarek, in neuronal networks by affecting targets beyond synapses. Here, we review the most Nencki Institute, Poland recent studies addressing the impact of extracellular proteolysis on plasticity of neuronal Reviewed by: excitability and discuss how enzymatic activity may alter input-output/transfer function Ania K. Majewska, University of Rochester, USA of neurons, supporting cognitive processes. Interestingly, extracellular proteolysis may Anna Elzbieta Skrzypiec, alter intrinsic neuronal excitability and excitation/inhibition balance both rapidly (time of University of Exeter, UK minutes to hours) and in long-term window.