To see the other types of publications on this topic, follow the link: Spine plasticity.
Dissertations / Theses on the topic 'Spine plasticity'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 dissertations / theses for your research on the topic 'Spine plasticity.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse dissertations / theses on a wide variety of disciplines and organise your bibliography correctly.
1
Critchlow, Hannah Marion. "The role of dendritic spine plasticity in schizophrenia." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612238.
Full text
2
Pfeiffer, Thomas. "Super-resolution STED and two-photon microscopy of dendritic spine and microglial dynamics." Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0743/document.
Full textAbstract:
Les changements des connections neuronales interviendraient dans la formation de la mémoire. J’ai développé de nouvelles approches basées sur l’imagerie photonique pour étudier (i) les interactions entre les microglies et les épines dendritiques, et (ii) le renouvellement des épines dans l’hippocampe in vivo. Ces deux phénomènes contribueraient au remodelage des circuits synaptiques intervenant dans la mémoire. (i) Les microglies sont impliquées dans de nouvelles fonctions en condition saine. J’ai examiné l’effet de la plasticité synaptique sur la dynamique morphologique des microglies, et sur leur interaction avec les épines. En combinant l’électrophysiologie et l’imagerie bi-photonique dans des tranches aigües de souris transgéniques, je démontre que la microglie intensifie son interaction physique avec les épines. Ainsi pour continuer l’étude de ces interactions et leur impact fonctionnel plus précisément, j’ai optimisé l’imagerie STED dans des tranches aigües. (ii) La plasticité structurale des épines est cruciale pour la mémoire, mais les connaissances à ce sujet dans l’hippocampe in vivo restent limitées. J’ai donc établi une technique d’imagerie chronique STED in vivo pour visualiser les épines dans l’hippocampe. Cette approche a révélé une densité double de celle reportée précédemment à l’aide de la microscopie bi-photonique. De plus j’ai observé un renouvellement des épines de 40% en 5 jours, représentant un taux important de remodelage synaptique dans l’hippocampe. Les approches d’imagerie super-résolutive permettent l’étude des interactions microglie-épine, et du renouvellement des épines hippocampiques avec une résolution inédite chez la souris vivante<br>Activity-dependent changes in neuronal connectivity are thought to underlie learning and memory. I developed and applied novel high-resolution imaging-based approaches to study (i) microglia-spine interactions and (ii) the turnover of dendritic spines in the mouse hippocampus, which are both thought to contribute to the remodeling of synaptic circuits underlying memory formation. (i) Microglia have been implicated in a variety of novel tasks beyond their classic immune defensive roles. I examined the effect of synaptic plasticity on microglial morphological dynamics and interactions with spines, using a combination of electrophysiology and two-photon microscopy in acute brain slices. I demonstrated that microglia intensify their physical interactions with spines after the induction of hippocampal synaptic plasticity. To study these interactions and their functional impact in greater detail, I optimized and applied time-lapse STED imaging in acute brain slices. (ii) Spine structural plasticity is thought to underpin memory formation. Yet, we know very little about it in the hippocampus in vivo, which is the archetypical memory center of the mammalian brain. I established chronic in vivo STED imaging of hippocampal spines in the living mouse using a modified cranial window technique. The super-resolution approach revealed a spine density that was two times higher than reported in the two-photon literature, and a spine turnover of 40% over 5 days, indicating a high level of structural remodeling of hippocampal synaptic circuits. The developed super-resolution imaging approaches enable the examination of microglia-synapse interactions and dendritic spines with unprecedented resolution in the living brain (tissue)
3
Chiang, Chih-Yuan. "Cortical development & plasticity in the FMRP KO mouse." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/22055.
Full textAbstract:
Autism is one of the leading causes of human intellectual disability (ID). More than 1% of the human population has autism spectrum disorders (ASDs), and it has been estimated that over 50% of those with ASDs also have ID. Fragile X syndrome (FXS) is the most common inherited form of mental retardation and is the leading known genetic cause of autism, affecting approximately 1 in 4000 males and 1 in 8000 females. Approximately 30% of boys with FXS will be diagnosed with autism in their later lives. The cause of FXS is through an over-expansion of the CGG trinucleotide repeat located at the 5’ untranslated region of the FMR1 gene, leading to hypermethylation of the surrounding sequence and eventually partially or fully silencing of the gene. Therefore, the protein product of the gene, fragile X mental retardation protein (FMRP), is reduced or missing. As a single-gene disorder, FXS offers a scientifically tractable way to examine the underlying mechanism of the disease and also shed some light on understanding ASD and ID. The mouse model of FXS (Fmr1−/y mice) is widely accepted and used as a good model, offering good structural and face validity. Since a primary deficit of FXS is believed to be altered neuronal communication, in this thesis I examined white matter tract and dendritic spine abnormalities in the mouse model of FXS. Loss of FMRP does not alter the gross morphology of the white matter. However, recent brain imaging studies indicated that loss of FMRP could lead to some minute abnormalities in different major white matter tracts in the human brain. The gross white matter morphology and myelination was unaltered in the Fmr1−/y mice, however, a small but significant increase of axon diameter in the corpus callosum (CC) was found compared to wild-type (WT) controls. Our computation model suggested that the increase of axon diameter in the Fmr1−/y mice could lead to an increase of conduction velocity in these animals. One of the key phenotypes reported previously in the loss of FMRP is the increase of “immature” dendritic spines. The increase of long and thin spines was reported in several brain regions including the somatosensory cortex and visual cortex in both FXS patients and the mouse model of FXS. Although recent studies which employed state-of-the-art microscopy techniques suggested that only minute differences were noticed between the WT and Fmr1−/y mice. In agreement with previous findings, I found an increase of dendritic spine density in the visual cortex in the Fmr1−/y mice, and spine morphology was also different between the two genotypes. We found that the spine head diameter is significantly increased in the CA1 area of the apical dendrites of the Fmr1−/y mice compared to WT controls. Dendritic spine length is also significantly increased in the same region of the Fmr1−/y mice. However, apical spine head size does not alter between the two genotypes in the V1 region of the visual cortex, and spine length is significantly decreased in the Fmr1−/y mice compared to WT animals in this region. Lovastatin, a drug known as one of the 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitors, functions as a modulator of the mitogen-activated protein kinases (MAPK) pathway through inhibiting Ras farnesylation, was used in an attempt to rescue the dendritic spine abnormalities in the Fmr1−/y mice. Mice lacking FMRP are susceptible to audiogenic seizure (AGS). Previous work has shown that 48 hr of lovastatin treatment reduced the incidence of AGS in the Fmr1−/y mice. However, chronic lovastatin treatment failed to rescue the spine density and morphology abnormalities in the Fmr1−/y mice. Mouse models are invaluable tools for modelling human diseases. However inter-strain differences have often confounded results between laboratories. In my final Chapter of this thesis, I compared two commonly used C57BL/6 substrains of mice by recording their electrophysiological responses to visual stimuli in vivo. I found a significant increase of high-frequency gamma power in adult C57BL/6JOla mice, and this phenomenon was reduced during the critical period. My results suggested that the C57BL/6JOla substrain has a significant stronger overall inhibitory network activity in the visual cortex than the C57BL/6J substrain. This is in good agreement with previous findings showing a lack of open-eye potentiation to monocular deprivation in the C57BL/6JOla substrain, and highlights the need for appropriate choice of mouse strain when studying neurodevelopmental models. They also give valuable insights into the genetic mechanisms that permit experience-dependent developmental plasticity. In summary, these findings give us a better understanding of the fine structure abnormalities of the Fmr1−/y mice, which in turn can benefit future discoveries of the underlying mechanisms of neurodevelopmental disorders such as ID and ASDs.
4
Coiro, Pierluca [Verfasser]. "Plasticity-related gene 5 induces spine formation in immature primary neurons / Pierluca Coiro." Berlin : Freie Universität Berlin, 2011. http://d-nb.info/1025355571/34.
Full text
5
Theis, Anne-Kathrin [Verfasser]. "Ryanodine receptor activation induces long-term plasticity of spine calcium dynamics / Anne-Kathrin Theis." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1119803357/34.
Full text
6
Knopp, Marcus. "Analysis of spine plasticity in CA1 hippocampal pyramidal neurons employing live cell nanoscopic imaging." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-173975.
Full textAbstract:
In der Großhirnrinde von Säugetieren befindet sich die Mehrheit erregender Synapsen auf Dornfortsätzen, kleinen dendritischen Ausbuchtungen, die in Größe und Form stark variieren. Die Auslösung aktivitätsabhängiger synaptischer Langzeitplastizität geht mit strukturellen Veränderungen dendritischer Dornen einher. Da das beugungsbegrenzte Auflösungsvermögen konventioneller Lichtmikroskope nicht ausreicht um die Morphologie der Dornen verlässlich zu untersuchen, stellte die Elektronenmikroskopie bisher das wichtigste bildgebende Verfahren zur Erforschung von struktureller Plastizität dar, blieb dabei jedoch auf die Betrachtung fixierter Gewebeproben beschränkt. Die Anwendung hochauflösender Laser-Raster-Mikroskopie mit Stimulierter-Emissions-Auslöschung hat es mir möglich gemacht, die Dynamik dendritischer Dornenmorphologie in lebenden Zellen zu studieren. Die N-Methyl-D-Aspartat-Rezeptor-abhängige Langzeitpotenzierung von Pyramidenzellen der Cornu-Ammonis Region 1 des Hippocampus bildete dabei den Mechanismus, welcher plastische Veränderungen hervorrief. Nach Potenzierung exzitatorischer Synapsen durch die lokale Ultraviolett-Photolyse von caged-Glutamat wurde ein starker, vorübergehender Anstieg des Anteils dendritischer Dornen mit sichelförmigen Köpfen und ein leichter, anhaltender Zuwachs an pilzförmigen Dornfortsätzen über einen Zeitraum von 50 Minuten beobachtet. Meine Untersuchungen ergänzen frühere Studien zur Wechselbeziehung zwischen synaptischer Potenzierung und struktureller Plastizität dendritischer Dornen und korrespondieren mit dem aktuellen Kenntnisstand der zu Grunde liegenden molekularen Mechanismen.<br>The majority of excitatory synapses in the cortex of mammalian brains is situated on dendritic spines, small protrusions, heterogeneous in size and shape. The induction of activity-dependent long-term synaptic plasticity has been associated with changes in the ultrastructure of spines, particularly in size, head shape and neck width. Since the dimensions of dendritic spines are at the border of the diffraction-limited resolving power of conventional light microscopes, until recently, electron microscopy on fixed tissue constituted the primary method for investigations on spine morphology. I have employed live cell stimulated emission depletion imaging to analyse spine motility and structural transitions in response to n-methyl-d-aspartate receptor dependent long-term potentiation over time at super-resolution in Cornu Ammonis area 1 pyramidal neurons of the hippocampus. Local induction of long-term potentiation via ultraviolet photolysis of caged glutamate facilitated a strong transient increase in the proportion of spines with curved heads and a subtle persistent growth in the amount of mushroom spines over a time course of 50 minutes. My findings reinforce previous investigations on the relation of synaptic potentiation and spine motility, and are in good agreement with the current knowledge of the molecular mechanisms underlying long-term plasticity.
7
O'Donnell, Cian. "Implications of stochastic ion channel gating and dendritic spine plasticity for neural information processing and storage." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/5886.
Full textAbstract:
On short timescales, the brain represents, transmits, and processes information through the electrical activity of its neurons. On long timescales, the brain stores information in the strength of the synaptic connections between its neurons. This thesis examines the surprising implications of two separate, well documented microscopic processes — the stochastic gating of ion channels and the plasticity of dendritic spines — for neural information processing and storage. Electrical activity in neurons is mediated by many small membrane proteins called ion channels. Although single ion channels are known to open and close stochastically, the macroscopic behaviour of populations of ion channels are often approximated as deterministic. This is based on the assumption that the intrinsic noise introduced by stochastic ion channel gating is so weak as to be negligible. In this study we take advantage of newly developed efficient computer simulation methods to examine cases where this assumption breaks down. We find that ion channel noise can mediate spontaneous action potential firing in small nerve fibres, and explore its possible implications for neuropathic pain disorders of peripheral nerves. We then characterise the magnitude of ion channel noise for single neurons in the central nervous system, and demonstrate through simulation that channel noise is sufficient to corrupt synaptic integration, spike timing and spike reliability in dendritic neurons. The second topic concerns neural information storage. Learning and memory in the brain has long been believed to be mediated by changes in the strengths of synaptic connections between neurons — a phenomenon termed synaptic plasticity. Most excitatory synapses in the brain are hosted on small membrane structures called dendritic spines, and plasticity of these synapses is dependent on calcium concentration changes within the dendritic spine. In the last decade, it has become clear that spines are highly dynamic structures that appear and disappear, and can shrink and enlarge on rapid timescales. It is also clear that this spine structural plasticity is intimately linked to synaptic plasticity. Small spines host weak synapses, and large spines host strong synapses. Because spine size is one factor which determines synaptic calcium concentration, it is likely that spine structural plasticity influences the rules of synaptic plasticity. We theoretically study the consequences of this observation, and find that different spine-size to synaptic-strength relationships can lead to qualitative differences in long-term synaptic strength dynamics and information storage. This novel theory unifies much existing disparate data, including the unimodal distribution of synaptic strength, the saturation of synaptic plasticity, and the stability of strong synapses.
8
Zhang, Shengxiang. "Imaging dendritic spine structural plasticity during development in vitro and after acute stroke in vivo." Thesis, University of British Columbia, 2006. http://hdl.handle.net/2429/31194.
Full textAbstract:
The plasticity of dendritic spine structure is important for neural development and synaptic function and is altered in many pathological conditions. In this study, we investigated the mechanisms underlying spine structural plasticity during development and the pathological changes in spine structure during ischemic stroke by using confocal and two-photon microscopy. We first investigated spine structural dynamics during development and the role of intracellular Ca²⁺ in determining basal spine motility in cultured hippocampal neurons. We found that young cultured neurons displayed significantly more spine motility than older neurons. In addition, we found that global buffering of intracellular Ca²⁺ failed to alter the basal motility of developing spines. Thus basal spine motility may represent an intrinsic feature of developing neurons and is not necessarily choreographed by ongoing changes in intracellular Ca²⁺ levels. We then examined spine structure changes during cerebral ischemia in vivo and investigated the relationships between cortical microcirculation and spine structure and function. We found moderate ischemia did not significantly affect spines within a 5-h time span; however, severe ischemia caused a rapid loss of spines and induced beading of dendrite structure within as little as 10 min following stroke. Surprisingly this damage was found to be reversible if reperfusion occurred within 20-60 min. By monitoring both cortical microcirculation and dendritic spine structure, we found that dendritic integrity deteriorated proportionally with the fraction of blocked vessels and the volume of affected brain during stroke. In ischemic border regions, we demonstrated that intact dendritic structure could be stably maintained for hours by blood flow from vessels that were on average 81 μm away. Functional imaging of intrinsic optical signals indicated that signal changes induced by limb movement were blocked in areas with blebbed dendrites, but were present at ~225 μm and beyond from the border of dendritic damage, suggesting peri-infarct tissues could function under acute ischemia in the core. In summary, our findings indicate that basal spine motility is maintained in a Ca²⁺ independent manner, and changes in spine structure during ischemia can now be directly linked to alterations in synaptic function and reductions in the cortical microcirculation.<br>Medicine, Faculty of<br>Graduate
9
Dhanrajan, T. M. "Morphological correlates of long-term potentiation and ageing in the hippocampus of rats." Thesis, Open University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340704.
Full text
10
Bauer, Rachel J. "THE EFFECTS OF LONG-TERM DEAFNESS ON DENSITY AND DIAMETER OF DENDRITIC SPINES ON PYRAMIDAL NEURONS IN THE DORSAL ZONE OF THE FELINE AUDITORY CORTEX." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/6028.
Full textAbstract:
Neuroplasticity has been researched in many different ways, from the growing neonatal brain to neural responses to trauma and injury. According to recent research, neuroplasticity is also prevalent in the ability of the brain to repurpose areas that are not of use, like in the case of a loss of a sense. Specifically, behavioral studies have shown that deaf humans (Bavalier and Neville, 2002) and cats have increased visual ability, and that different areas of the auditory cortex enhance specific kinds of sight. One such behavioral test demonstrated that the dorsal zone (DZ) of the auditory cortex enhances sensitivity to visual motion through cross-modal plasticity (Lomber et. al., 2010). Current research seeks to examine the anatomical structures responsible for these changes through analysis of excitatory neuron dendritic spine density and spine head diameter. This present study focuses on the examination of DZ neuron spine density, distribution, and size in deaf and hearing cats to corroborate the visual changes seen in behavioral studies. Using Golgi-stained tissue and light microscopy, our results showed a decrease in overall spine density but slight increase in spine head diameter in deaf cats compared to hearing cats. These results, along with several other studies, support multiple theories on how cross-modal reorganization of the auditory cortex occurs after deafening
11
Robertson, Holly Rochelle. "Regulation of dendritic spine structure and function by A-kinase anchoring protein 79/150 /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2008.
Find full textAbstract:
Thesis (Ph.D. in Pharmacology) -- University of Colorado Denver, 2008.<br>Typescript. Includes bibliographical references (leaves 135-162). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
12
Knopp, Marcus Verfasser], and Tobias [Akademischer Betreuer] [Bonhoeffer. "Analysis of spine plasticity in CA1 hippocampal pyramidal neurons employing live cell nanoscopic imaging / Marcus Knopp. Betreuer: Tobias Bonhoeffer." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1059351234/34.
Full text
13
Hamel, Michelle Grace. "Modulation of neural plasticity by the ADAMTSs (a disintegrin and metalloproteinase with thrombospondin motifs)." [Tampa, Fla] : University of South Florida, 2006. http://purl.fcla.edu/usf/dc/et/SFE0001684.
Full text
14
Amini, Mandana. "Analysis of Conditional Knock-out of Calpain Small Subunit, capns1, in Central Nervous System Development and Function." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31360.
Full textAbstract:
Calpains, a highly conserved family of calcium-dependent cysteine proteases, are divided in two groups; classical and non-conventional calpains. Calpain-1 and calpain-2, the classical ones, are ubiquitously expressed and abundant in the CNS. Findings through different experimental approaches, predominantly pharmacological calpain inhibitors, proposed the necessity of the proteases for the modulation of various biological events particularly in the CNS, or a functional link between calpain and neurodegeneration. Significant functions associated with calpain activity are neuronal proliferation/differentiation, signal transduction, apoptosis, and synaptic plasticity; or neuronal death in Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and ischemic stroke. However, due to limited insights of the approaches taken, such as non-specificity of the inhibitors, the exact roles of calpains in the CNS and the key mechanisms underlying them remain controversial. Calpain-1/calpain-2 germline knock-out are embryonic lethal at a very early stage hindering the use of these lines as mouse models for CNS studies. Accordingly, this thesis research introduced a unique brain-specific calpain-1/calpain-2 knock-out and explored the role of the proteases in brain development/function and in neuronal death. The first set of analyses examined how the elimination of calpain-1/calpain-2 activities in mouse brain impacts CNS development in general and synaptic plasticity in CA1 neurons of hippocampus. CNS-specific elimination of CAPNS1, the common small subunit, abolished calpain-1/calpain-2 activities in mouse brain. In contrast to Calpain-1/calpain-2 germ line knock-outs, the brain-specific knock-outs are viable and the general development of mouse brain is normal. However, morphology of dendrites in pyramidal neurons of the hippocampal CA1 region showed significantly decreased dendritic branching complexity and spine density. Consistent with dendrite morphological abnormalities, electrophysiological analyses revealed a significant decrease in field excitatory postsynaptic potentials, long term potentiation, and learning and memory in the hippocampal CA1 neurons of the mutants. In the second part of this research we investigated the direct role of the calpains in neuronal death and their potential downstream targets in in vitro models of PD and ischemic stroke. Our findings indicated that ablation of calpains activity improves survival of different types of neurons against mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP+), glutamate, and hypoxia. Importantly, we demonstrated an increase in p35-cleavage to p25, a cyclin dependent kinase 5 (Cdk5) activator, and that restoration of p25 significantly suppresses the neuronal survival associated with calpain deficiency. Taken together, this work unequivocally establishes two central roles of calpain-1/calpain-2 in CNS function in plasticity and neuronal death.
15
Scharkowski, Franziska Verfasser], and Martin [Akademischer Betreuer] [Korte. "Spine development and activity-dependent plasticity in the hippocampus of a mouse model of the fragile X syndrome / Franziska Scharkowski ; Betreuer: Martin Korte." Braunschweig : Technische Universität Braunschweig, 2017. http://d-nb.info/1175818003/34.
Full text
16
Chen, Jian Hua [Verfasser], Peter Jomo [Akademischer Betreuer] Walla, Reinhard [Akademischer Betreuer] Jahn, and Andreas [Akademischer Betreuer] Janshoff. "Spatial-temporal actin dynamics during synaptic plasticity of single dendritic spine investigated by two-photon fluorescence correlation spectroscopy / Jian Hua Chen. Gutachter: Reinhard Jahn ; Andreas Janshoff. Betreuer: Peter Jomo Walla." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2013. http://d-nb.info/1045776246/34.
Full text
17
Chen, Jian Hua Verfasser], Peter Jomo [Akademischer Betreuer] [Walla, Reinhard [Akademischer Betreuer] Jahn, and Andreas [Akademischer Betreuer] Janshoff. "Spatial-temporal actin dynamics during synaptic plasticity of single dendritic spine investigated by two-photon fluorescence correlation spectroscopy / Jian Hua Chen. Gutachter: Reinhard Jahn ; Andreas Janshoff. Betreuer: Peter Jomo Walla." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2013. http://nbn-resolving.de/urn:nbn:de:gbv:7-11858/00-1735-0000-0022-609F-1-7.
Full text
18
Mendes, Alexandre. "Homo- et hétérosynaptique spike-timing-dependent plasticity aux synapses cortico- et thalamo-striatales." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066432/document.
Full textAbstract:
D’après le postulat de Hebb, les circuits neuronaux ajustent et modifient durablement leurs poids synaptiques en fonction des patrons de décharges de part et d’autre de la synapse. La « spike-timing-dependent plasticity » (STDP) est une règle d’apprentissage synaptique hebbienne dépendante de la séquence temporelle précise (de l’ordre de la milliseconde) des activités appariées des neurones pré- et post-synaptiques. Le striatum, le principal noyau d’entrée des ganglions de la base, reçoit des afférences excitatrices provenant du cortex cérébral et du thalamus dont les activités peuvent être concomitantes ou décalées dans le temps. Ainsi, l’encodage temporal des informations corticales et thalamiques via la STDP pourrait être crucial pour l’implication du striatum dans l’apprentissage procédural. Nous avons exploré les plasticités synaptiques cortico- et thalamo-striatales puis leurs interactions à travers le paradigme de la STDP. Les principaux résultats sont :1. Les « spike-timing-dependent plasticity » opposées cortico-striatales et thalamo-striatales induisent des plasticités hétérosynaptiques. Si la très grande majorité des études sont consacrées à la plasticité synaptique cortico-striatale, peu ont exploré les règles de plasticité synaptique aux synapses thalamo-striatale et leurs interactions avec la plasticité cortico-striatale. Nous avons étudié la STDP thalamo-striatale et comment les plasticités synaptiques thalamo- et cortico-striatales interagissent…<br>According to Hebbian postulate, neural circuits tune their synaptic weights depending on patterned firing of action potential on either side of the synapse. Spike-timing-dependent plasticity (STDP) is an experimental implementation of Hebbian plasticity that relies on the precise order and the millisecond timing of the paired activities in pre- and postsynaptic neurons. The striatum, the primary entrance to basal ganglia, integrates excitatory inputs from both cerebral cortex and thalamus whose activities can be concomitant or delayed. Thus, temporal coding of cortical and thalamic information via STDP paradigm may be crucial for the role of the striatum in procedural learning. Here, we explored cortico-striatal and thalamo-striatal synaptic plasticity and their interplay through STDP paradigm. The main results described here are:1. Opposing spike-timing dependent plasticity at cortical and thalamic inputs drive heterosynaptic plasticity in striatumIf the vast majority of the studies focused on cortico-striatal synaptic plasticity, much less is known about thalamo-striatal plasticity rules and their interplay with cortico-striatal plasticity. Here, we explored thalamo-striatal STDP and how thalamo-striatal and cortico-striatal synaptic plasticity interplay. a) While bidirectional and anti-Hebbian STDP was observed at cortico-striatal synapses, thalamo-striatal exhibited bidirectional and hebbian STDP
19
Blair, Jeffrey A. "Luteinizing hormone in the central nervous system: a direct role in learning and memory." Kent State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=kent1523397060445531.
Full text
20
Margarido, Pinheiro Vera. "L’interactome de Scrib1 et son importance pour la plasticitè synaptique & les troubles de neurodéveloppement." Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0318/document.
Full textAbstract:
Le cerveau contient environ cent milliards de cellules nerveuses, ou neurones. Ces neurones communiquent entre eux par des structures fonctionnellement distinctes – l’axone et la dendrite – capables d’émettre et recevoir des signaux électriques ou chimiques à partir d’un compartiment présynaptique vers un compartiment, dit post-synaptique. Nous avons focalisé notre étude sur les synapses des neurones hippocampiques, qu’on estime responsables de fonctions cérébrales dites supérieures, comme la mémoire et l’apprentissage. Plus particulièrement, on s’est intéressé au développement et au maintien des épines dendritiques, dont les changements morphologiques sont intimement liés à la plasticité synaptique, autrement dit, capacité de réponse à l’activité synaptique. Les épines dendritiques ont pour origine les filopodes qui évoluent en épines lors du contact axonal. La transition entre filopode et épine implique une myriade de molécules, dont des récepteurs glutamatergiques, des protéines d’échafaudage et du cytosquelette d’actine capables de recevoir, transmettre et intégrer le signal présynaptique. Cependant, la coordination spatiale et temporelle de tous ces composants moléculaires au long de la formation et maturation d’une synapse reste largement méconnue.Scribble1 (Scrib1) est une protéine de polarité cellulaire (PCP) classiquement impliquée dans l’homéostasie de tissues épithéliaux ainsi que dans la croissance et progression des tumeurs. Scrib1 est aussi une protéine d’échafaudage critique pour le développement et le bon fonctionnement du cerveau. L’objectif de cette étude a donc été d’étudier les mécanismes moléculaires sous-jacents à un rôle potentiel de Scrib1 dans la formation et le maintien des synapses. Dans un premier temps, on a décrit l’importance d’interactions dépendantes des domaines PDZ sur le trafic des récepteurs glutamatergiques ainsi que sur la voie de signalisation de plasticité synaptique sous-jacente à la mémoire spatiale. Dans un second temps, nous avons évalué les conséquences fonctionnelles d’une mutation de Scrib1 récemment identifiée chez un patient humain atteint des troubles du spectre autistique (TSA) dans la morphologie et fonction des neurones. On a démontré que Scrib1 régule l’arborisation dendritique ainsi que la formation et le maintien fonctionnel des épines dendritiques via un mécanisme dépendent du cytosquelette d’actine. Le dérèglement de ces mécanismes pourrait être à l’origine du phénotype TSA. L’ensemble de ce travail met en évidence que Scrib1, protéine d’échafaudage clé dans le développement et la fonction du cerveau, joue une multitude de rôle du niveau subcellulaire au niveau cognitif<br>The brain is made up of billions of nerve cells, or neurons. Neurons communicate with each other through functionally distinct structures - the axon and the dendrite - which are able to release and receive an electrical or chemical signal from a pre- to a post-synaptic compartment, respectively. We focused our study on hippocampal neurons synapses, which ultimately underlie high-order brain functions, such as learning and memory. In particular, we studied the development and maintenance of dendritic spines, whose changes in morphology are intimately correlated with synaptic plasticity, or the ability to respond to synaptic activity. Dendritic spines originate from motile dendritic filopodia, which mature into spines following axonal contact. The filopodia-to-spine transition involves a plethora of molecular actors, including glutamate receptors, scaffold proteins and the actin cytoskeleton, able to receive, transmit and integrate the pre-synaptic signal. The spatial and temporal coordination of all these molecular components throughout the formation and maturation of a synapse remains, however, unclear. Scribble1 (Scrib1) is planar cell polarity protein (PCP) classically implicated in the homeostasis of epithelial tissues and tumour growth. In the mammalian brain, Scrib1 is a critical scaffold protein in brain development and function. The main goal of this work was, therefore, to investigate the molecular mechanisms underlying Scrib1 role in synapse formation and maintenance. In a first part, we depict the importance of Scrib1 PDZ-dependent interactions on glutamate receptors trafficking as well as bidirectional plasticity signalling pathway underying spatial memory. In a second part, we focus on the functional consequences of a recently identified autism spectrum disorder (ASD) mutation of Scrib1 on neuronal morpholgy and function. We demonstrated that Scrib1 regulates dendritic arborization as well as spine formation and functional maintenance via an actin-dependent mechanism, whose disruption might underlie the ASD phenotype. Taken altogether, this thesis highlights the PCP protein Scrib1 as key scaffold protein in brain development and function, playing a plethora of roles from the subcelular to the cognitive level
21
Leiss, Florian. "Dendritic spines and structural plasticity in Drosophila." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-104626.
Full text
22
Prokin, Ilia. "Synaptic plasticity emerging from chemical reactions : Modeling spike-timing dependent plasticity of basal ganglia neurons." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSEI115/document.
Full textAbstract:
Notre cerveau prend en charge différentes formes d’apprentissage dans ses diverses parties. C’est par exemple le cas des ganglions de la base, un ensemble de noyaux sous-corticaux qui est impliqué dans la sélection de l’action et une forme spécifique de l’apprentissage / mémoire, la mémoire procédurale (mémoire des compétences ou d’expertise). A l’échelle du neurone unique, le support le plus plausible de l’apprentissage et de la mémoire est la plasticité synaptique, le processus par lequel l’efficacité de la communication entre deux neurones change en réponse à un pattern spécifique de conditions environnementales. Parmi les différentes formes de plasticité synaptique, la plasticité dépendante du timing des spikes (STDP) représente le fait que le poids synaptique (l’efficacité de la connexion) change en fonction du temps écoulé entre l’émission des deux potentiels d’action (spikes) présynaptiques et postsynaptiques consécutifs. Si la STDP est une forme de plasticité qui a récemment attiré beaucoup d’intérêt, on ne comprend pas encore comment elle émerge des voies de signalisation / biochimiques qui la sous-tendent. Pour répondre à cette question, nous combinons les approches expérimentales de nos collaborateurs (pharmacologie et électrophysiologie) avec la modélisation de la dynamique des réseaux de signalisation impliquées (décrite par des équations différentielles ordinaires). Après estimation des paramètres, le modèle reproduit la quasi-totalité des données expérimentales, y compris la dépendance de la STDP envers le nombre stimulations pré- et post-synaptiques appariées et son exploration pharmacologique intensive (perturbation des voies de signalisation par des produits chimiques). En outre, contrairement à ce qui était largement admis dans la communauté des neurosciences, notre modèle indique directement que le système endocannabinoïde contrôle les changements du poids synaptique de façon bi-directionnelle (augmentation et diminution). De plus, nous étudions comment une série de facteurs comme la recapture du glutamate régule la STDP. Notre modèle représente une première étape pour l’élucidation de la régulation de l’apprentissage et de la mémoire au niveau du neurone unique dans les ganglions de la base<br>Our brains support various forms of learning in their various subparts. This is for instance the case of the basal ganglia, a set of subcortical nuclei that is involved in action selection and a specific form of learning / memory, procedural memory (memory of skills or expertise). At the scale of single neurons, the most plausible support of learning and memory is synaptic plasticity, the process by which the efficiency of interneuronal communication changes in response to a pattern of environmental conditions. A recent focus of research is on spike-timing dependent plasticity (STDP), whereby the relative timing of activations (spikes) of connected pre- and postsynaptic neurons, determines the synaptic weight (the efficiency of synaptic connection). Notwithstanding, the dependence of STDP on underlying signaling pathways is not yet fully understood. To address this issue, we combine experimental approaches by our collaborators (pharmacology and electrophysiology) with modeling of the implicated signaling network (described by Ordinary-Differential Equations). After parameter estimation, the model reproduces much of experimental data, including the dependence of STDP on the number of paired stimuli of pre- and postsynaptic neurons and intensive pharmacological exploration (where signaling molecules are perturbed by chemicals). Furthermore, in opposition to what was widely believed in the neuroscience community, our model directly indicates that the endocannabinoid system supports bidirectional changes of the synaptic weight (increase and decrease). Moreover, we study how a range of factors including glutamate uptake regulates STDP. We expect our model to be a starting point to the elucidation of the regulation of learning and memory in the basal-ganglia at the single neuron level
23
Liu, Daqi. "Deep visual learning with spike-timing dependent plasticity." Thesis, University of Lincoln, 2017. http://eprints.lincoln.ac.uk/28660/.
Full textAbstract:
For most animal species, reliable and fast visual pattern recognition is vital for their survival. Ventral stream, a primary pathway within visual cortex, plays an important role in object representation and form recognition. It is a hierarchical system consisting of various visual areas, in which each visual area extracts different level of abstractions. It is known that the neurons within ventral stream use spikes to represent these abstractions. To increase the level of realism in a neural simulation, spiking neural network (SNN) is often used as the neural network model. From SNN point of view, the analog output values generated by traditional artificial neural network (ANN) can be considered as the average spiking firing rates. Unlike traditional ANN, SNN can not only use spiking rates but also specific spiking timing sequences to represent the structural information of the input visual stimuli, which greatly increases the distinguishability. To simulate the learning procedure of the ventral stream, various research questions need to be resolved. In most cases, traditional methods use winner-take-all strategy to distinguish different classes. However, such strategy works not well for overlapped classes within decision space. Moreover, neurons within ventral stream tends to recognize new input visual stimuli in a limited time window, which requires a fast learning procedure. Furthermore, within ventral stream, neurons receive continuous input visual stimuli and can only access local information during the learning procedure. However, most traditional methods use separated visual stimuli as the input and incorporate global information within the learning period. Finally, to verify the universality of the proposed SNN framework, it is necessary to investigate its classification performance for complex real world tasks such as video-based face disguise recognition. To address the above problems, a novel classification method inspired by the soft I winner-take-all strategy has been proposed firstly, in which each associated class will be assigned with a possibility and the input visual stimulus will be classified as the class with the highest possibility. Moreover, to achieve a fast learning procedure, a novel feed-forward SNN framework equipped with an unsupervised spike-timing dependent plasticity (STDP) learning rule has been proposed. Furthermore, an eventdriven continuous STDP (ECS) learning method has been proposed, in which two novel continuous input mechanisms have been used to generate a continuous input visual stimuli and a new event-driven STDP learning rule based on the local information has been applied within the training procedure. Finally, such methodologies have also been extended to the video-based disguise face recognition (VDFR) task in which human identities are recognized not just on a few images but the sequences of video stream showing facial muscle movements while speaking.
24
Billings, Guy. "Memory stability and synaptic plasticity." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/3853.
Full textAbstract:
Numerous experiments have demonstrated that the activity of neurons can alter the strength of excitatory synapses. This synaptic plasticity is bidirectional and synapses can be strengthened (potentiation) or weakened (depression). Synaptic plasticity offers a mechanism that links the ongoing activity of the brain with persistent physical changes to its structure. For this reason it is widely believed that synaptic plasticity mediates learning and memory. The hypothesis that synapses store memories by modifying their strengths raises an important issue. There should be a balance between the necessity that synapses change frequently, allowing new memories to be stored with high fidelity, and the necessity that synapses retain previously stored information. This is the plasticity stability dilemma. In this thesis the plasticity stability dilemma is studied in the context of the two dominant paradigms of activity dependent synaptic plasticity: Spike timing dependent plasticity (STDP) and long term potentiation and depression (LTP/D). Models of biological synapses are analysed and processes that might ameliorate the plasticity stability dilemma are identified. Two popular existing models of STDP are compared. Through this comparison it is demonstrated that the synaptic weight dynamics of STDP has a large impact upon the retention time of correlation between the weights of a single neuron and a memory. In networks it is shown that lateral inhibition stabilises the synaptic weights and receptive fields. To analyse LTP a novel model of LTP/D is proposed. The model centres on the distinction between early LTP/D, when synaptic modifications are persistent on a short timescale, and late LTP/D when synaptic modifications are persistent on a long timescale. In the context of the hippocampus it is proposed that early LTP/D allows the rapid and continuous storage of short lasting memory traces over a long lasting trace established with late LTP/D. It is shown that this might confer a longer memory retention time than in a system with only one phase of LTP/D. Experimental predictions about the dynamics of amnesia based upon this model are proposed. Synaptic tagging is a phenomenon whereby early LTP can be converted into late LTP, by subsequent induction of late LTP in a separate but nearby input. Synaptic tagging is incorporated into the LTP/D framework. Using this model it is demonstrated that synaptic tagging could lead to the conversion of a short lasting memory trace into a longer lasting trace. It is proposed that this allows the rescue of memory traces that were initially destined for complete decay. When combined with early and late LTP/D iii synaptic tagging might allow the management of hippocampal memory traces, such that not all memories must be stored on the longest, most stable late phase timescale. This lessens the plasticity stability dilemma in the hippocampus, where it has been hypothesised that memory traces must be frequently and vividly formed, but that not all traces demand eventual consolidation at the systems level.
25
Cui, Yihui. "The many faces of corticostriatal spike-timing dependent plasticity." Paris 6, 2013. http://www.theses.fr/2013PA066398.
Full textAbstract:
La plasticité corticostriatale est le substrat de l’apprentissage procédural. Nous avons caractérisé l’implication des endocannabinoides (eCBs) dans des formes de plasticité non-hebiennes telle que la depolarization-induced suppression of excitation (DSE) ou les stimulations à basse fréquence. Nous nous sommes ensuite concentré sur la caractérisation de la spike timing-dependent plasticity (STDP). Nous avons démontré que la LTP-STDP etait NMDAR dépendante alors que la LTD de��pendait des eCBs. En baissant le nombre de stimulations nous avons mis en évidence une nouvelle forme de plasticité: une eCB-LTP induite par un très faible nombre de stimulations appariées (5-10). Cette eCB-LTP est homosynaptique, médiée par l’activation des récepteurs CB1 et TRPV1 et par le couple présynaptique PKA-calcineurine. Nos résultats démontrent le large spectre d’action des eCBs puisque ceux-ci sous-tendent non seulement les phénomènes de dépression synaptique mais aussi de potentiation. Nous avons alors exploré les limites de la STDP en variant la fréquence des stimulations corticostriatales et observé une transition entre la dépendance au timing vs fréquence de la STDP dans laquelle la LTP est médiée par les NMDAR (pour de faibles fréquences) puis par un mélange NMDAR / CB1R (pour des fréquences plus élevées). Enfin, nous avons montré une très sensibilité des plasticités NMDA-dépendantes face au jitter alors que celles médiées par les eCBs sont beaucoup plus résistantes au jitter. Ces résultats montrent de nouvelles formes de plasticités corticostriatales et la grande complexité des règles d’apprentissage synaptiques qui gouvernent le traitement des informations corticostriatales<br>The corticostriatal plasticity is thought to be the neuronal substrate of procedural learning. We first investigated non-hebbian plasticity and found that both depolarization-induced suppression of excitation (DSE) and low-frequency stimulation (LFS) protocols induced LTD and are both mediated by endocannabinoid (eCB)-signaling. We then focused on corticostriatal spike timing-dependent plasticity (STDP) characterization and robustness. We found that with 100 STDP pairings, corticostriatal LTP was NMDA-dependent while LTD involved eCB-signaling. We then tested the robustness of corticostriatal STDP. We uncovered that LTP was even inducible with 5 pairings. Thanks to a model-driven experiment strategy, we demonstrated that this LTP relies on eCB-signaling. This eCB-LTP is homosynaptic, depends on cannabinoid-type-1 receptor (CB1R) and transient receptor potential vanilloid-type-1 (TRPV1) activation and is supported by presynaptic PKA and calcineurin. Our results considerably enlarge the spectrum of action of eCBs since they show that eCBs promote not only depression but also potentiation. To investigate the limits of corticostriatal STDP, we varied the STDP rate. We observed a transition from timing- to rate-dependent plasticity. This rate-dependency exists with both 100 and 10 pairings, in which LTP is respectively NMDA-dependent and CB1 and NMDA receptors. We then applied a randomized jitter within STDP protocol. We showed that NMDA-LTP is highly sensitive to jitter while eCB-LTP is not. These results showed novel forms of corticostriatal plasticity and demonstrated that the multiple learning rules at play for governing the corticostriatal information processing
26
Waddington, Amelia. "Growing synfire chains with triphasic spike-time-dependent plasticity." Thesis, University of Leeds, 2011. http://etheses.whiterose.ac.uk/1758/.
Full textAbstract:
How collections of neurons combine into functional networks capable of intricate and accurate information processing is one of the biggest and most interesting challenges in neuroscience today. To approach this challenge, it is necessary to address the problem one structure at a time. In this thesis the focus is the development of synfire chains. Synfire chains are feed-forward neural structures which have long been suggested as a possible mechanism by which precisely timed sequences of neural activity could be generated. Precise spatiotemporal firing patterns are known to occur in the brains of many animals including, rats, mice, song birds, monkeys and humans. Such firing patterns have been linked with a wide range of behaviours including motor responses and sensory encoding. There have been many previous computational studies which address the development of synfire chains. However, they have all required either initial sparse connectivity or strong topological constraints in addition to any synaptic learning rules. Here, it is shown that this necessity can be removed. In this model, development is guided by an experimentally reported spike-timing-dependent plasticity (STDP) rule, triphasic STDP, plus activity-dependent excitability. This STDP rule, which has not been previously used in computational studies, is shown to successfully develop a synfire chain in a network of binary neurons. The width and length of the final chain can be controlled through model parameters. In addition, it is possible to embed multiple chains within one neural network. Next, the effect of triphasic STDP is investigated in a network of more realistic leaky integrate and fire neurons. Here, synfire chain development is shown to be robust in the presence of heterogeneous delays. Finally, the development is described as a random walk, creating a concrete relationship between the model parameters and final network structure.
27
René, Alice. "Plasticité synaptique et fonctionnelle dans le cortex visuel primaire : une étude par conditionnement theta - burst in vivo." Paris 6, 2007. http://www.theses.fr/2007PA066656.
Full textAbstract:
Des bouffées à 100 Hz répétées à la fréquence theta - burst dans les afférents thalamiques peuvent-elles induire des modifications synaptiques et affecter l'organisation des champs récepteurs visuels (CR) des neurones corticaux in vivo ? Des enregistrements intracellulaires dans l'aire 17 du chat adulte ont été réalisés ainsi que la stimulation et l'enregistrement extracellulaire du CGL. Les réponses à la stimulation électrique du CGL (PSP) sont potentialisées (50%) ou déprimées (32%) par theta - burst. Des modifications sélectives des CRs sont observés dans 40% des cas, sont spécifiques de la localisation du CR des entrées thalamiques et montrent une anisotropie en accord avec le signe du changement du PSP. Les modifications synaptiques suivent une règle de plasticité associative proche d'une détection de coïncidence et l'ordre temporel entre activité pré- et post-synaptique importe moins que le contexte post-synaptique de dépolarisation et d'inhibition présente au moment de la décharge.
28
Eberhorn, Nicola. "Functional and Morphological Plasticity of Dendritic Spines in the Hippocampus." Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-47751.
Full text
29
Oliveira, Alexandre (Alexandre S. ). "Finding patterns in timed data with spike timing dependent plasticity." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/77031.
Full textAbstract:
Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2012.<br>Cataloged from PDF version of thesis.<br>My research focuses on finding patterns in events - in sequences of data that happen over time. It takes inspiration from a neuroscience phenomena believed to be deeply involved in learning. I propose a machine learning algorithm that finds patterns in timed data and is highly robust to noise and missing data. It can find both coincident relationships, where two events tend to happen together; as well as causal relationships, where one event appears to be caused by another. I analyze stock price information using this algorithm and strong relationships are found between companies within the same industry. In particular, I worked with 12 stocks taken from the banking, information technology, healthcare, and oil industries. The relationships are almost exclusively coincidental, rather than causal.<br>by Alexandre Oliveira.<br>M.Eng.
30
Monzon, Joshua Jen C. "Analog VLSI circuit design of spike-timing-dependent synaptic plasticity." Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/54636.
Full textAbstract:
Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2008.<br>Cataloged from PDF version of thesis.<br>Includes bibliographical references (p. 61-63).<br>Synaptic plasticity is the ability of a synaptic connection to change in strength and is believed to be the basis for learning and memory. Currently, two types of synaptic plasticity exist. First is the spike-timing-dependent-plasticity (STDP), a timing-based protocol that suggests that the efficacy of synaptic connections is modulated by the relative timing between presynaptic and postsynaptic stimuli. The second type is the Bienenstock-Cooper-Munro (BCM) learning rule, a classical ratebased protocol which states that the rate of presynaptic stimulation modulates the synaptic strength. Several theoretical models were developed to explain the two forms of plasticity but none of these models came close in identifying the biophysical mechanism of plasticity. Other studies focused instead on developing neuromorphic systems of synaptic plasticity. These systems used simple curve fitting methods that were able to reproduce some types of STDP but still failed to shed light on the biophysical basis of STDP. Furthermore, none of these neuromorphic systems were able to reproduce the various forms of STDP and relate them to the BCM rule. However, a recent discovery resulted in a new unified model that explains the general biophysical process governing synaptic plasticity using fundamental ideas regarding the biochemical reactions and kinetics within the synapse. This brilliant model considers all types of STDP and relates them to the BCM rule, giving us a fresh new approach to construct a unique system that overcomes all the challenges that existing neuromorphic systems faced. Here, we propose a novel analog verylarge- scale-integration (aVLSI) circuit that successfully and accurately captures the whole picture of synaptic plasticity based from the results of this latest unified model. Our circuit was tested for all types of STDP and for each of these tests, our design was able to reproduce the results predicted by the new-found model. Two inputs are required by the system, a glutamate signal that carries information about the presynaptic stimuli and a dendritic action potential signal that contains information about the postsynaptic stimuli. These two inputs give rise to changes in the excitatory postsynaptic current which represents the modifiable synaptic efficacy output. Finally, we also present several techniques and alternative circuit designs that will further improve the performance of our neuromorphic system.<br>by Joshua Jen C. Monzon.<br>M.Eng.
31
Jacob, Vincent. "Intégration spatio-temporelle de scènes tactiles et plasticité fonctionnelle dans le cortex à tonneaux du rat." Paris 6, 2007. http://www.theses.fr/2007PA066222.
Full textAbstract:
Classiquement, les connexions entre vibrisses et tonneaux corticaux sont considérées comme des voies indépendantes. Cependant le rat génère des contacts multiples lors de l'exploration active. Les champs récepteurs (CR) corticaux sont très étendus, suggérant qu'une information multivibrissale converge sur chaque neurone. Afin d'étudier l'intégration de scènes tactiles dans le cortex, nous avons développé une matrice de 25 stimulateurs qui nous a permis d’étudier les CRs, leur dépendance à l’omission d’un stimulus prédictible et la sélectivité à la direction générale générée par la déflection séquentielle des vibrisses. Le cortex primaire réalise donc une analyse intégrée non-linéaire de l’information sensorielle. Certaines conditions d’activité engendrent une modification durable des CRs. Nous avons observé des modifications de réponse sensorielle dont le signe et l’intensité dépendent de l’ordre et de l’intervalle de temps entre la stimulation et l'activation post-synaptique du neurone enregistré, résultat compatible avec les règles de STDP pour lesquelles ce travail constitue la première validation dans le cortex somatosensoriel in vivo<br>Classically the connections between whiskers and cortical barrels are considered as independent ways. However, the rat generates complex patterns of contacts during active exploration. The cortical receptive fields (RF) are very large suggesting that multiwhisker information converge on each neuron. In order to study the integration of tactile scenes in the cortex, we have developed a matrix of 25 stimulators. We studied the RFs, their dependence to the omission of a predictable stimulus and the selectivity to global direction generated by sequential deflections of the whiskers. Then primary cortex performs an integrated and non-linear analysis of sensory information. Conditions of activity induce long-term modifications of the RFs. We observed modifications of the sensory response whose sign and intensity depended on the order and the time interval between the stimulations and the post-synaptic activation of the recorded neuron. This result is compatible with STDP rules for which this work is the first validation in the in vivo somatosensory cortex
32
Strain, Thomas. "A spiking neuron training approach using spike timing-dependent plasticity (STDP)." Thesis, Ulster University, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538954.
Full textAbstract:
Spiking Neural Networks (SNNs) model the dynamics and learning capabilities of the brain in a more biologically inspired way than previous generations of neural networks. However, training these networks is still problematic due to over-training and weight instabilities. This research focuses on the design and implementation of a more biologically inspired training algorithm, based on the Spike Timing Dependent Plasticity (STDP) learning rule where weight changes are dependant on the temporal distribution of the input data; the algorithm cross correlates (CC) similarities in the input data across all classes and hence implements global training. The implementation required that the original STDP training rule be extended to take into account both global and local similarities in the input data across all classes. Other novel features of the approach are the use of multiple synaptic connections, axonal delays and dynamic thresholds. Results from the benchmark problems, Iris and Wisconsin Breast Cancer data, for two and three layer SNNs are presented. The three layer SNN has showed a classification accuracy which was superior to the two layer network and comparable to other approaches. Unlike the two layer SNN, the three layer structure utilised the CC rule together with dynamic thresholds where the latter correlated similarities in the spatial patterns across the different data classes. Further investigations were carried out on a temporal application, speech corpus TI46 data. The TI46 data was pre-processed using the most popularly applied method: Mel-Frequency Cepstral Coefficients (MFCC). The results obtained are highly comparable with results from more complex state-of-the-art classification systems such as Liquid State Machines. The proposed learning algorithm facilitates competition between neurons eradicating the problem of a bi-polar weight distribution, consequently stabilising learning. Results have demonstrated that this novel learning technique produces stability in the learning process and is a significant contribution in enabling SNNs to be applied to realistic real world classification problems.
33
Appleby, Peter A. "A synaptic and temporal ensemble interpretation of spike-timing-dependent plasticity." Thesis, University of Southampton, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427459.
Full text
34
Soltani, Asma. "Etude de l’expression de l'homéoprotéine Engrailed dans l’hippocampe et de ses effets sur la complexité dendritique." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05T006/document.
Full textAbstract:
Engrailed (En) est un facteur de transcription important pour la mise en place de la segmentation de l’embryon et du plan d’organisation antéro-postérieur. Comme d’autres membres de la famille des homéoprotéines, Engrailed peut aussi agir comme une molécule de signalisation extracellulaire, internalisable grâce à son domaine « pénétratine » et stimulant dans la cellule cible la transcription ou la traduction des ARNm. De cette façon, Engrailed guide les axones en modifiant la traduction dans le cône de croissance axonal et l’infusion cérébrale d’Engrailed protège les neurones dopaminergiques dans un modèle de la maladie de Parkinson en augmentant la traduction de protéines mitochondriales. Des troubles cognitifs et un déficit des interactions sociales ont été observés chez les souris En1+/- et les souris En2-/-. Une augmentation de l’expression d’En2 a aussi été observée chez des patients atteints de troubles du spectre autistique. Néanmoins, le lien entre les modifications de l’expression d’Engrailed et l’autisme ne sont pas compris. L’objectif de cette thèse a été d’étendre notre connaissance des fonctions d’Engrailed dans une région télencéphalique où elle est a priori peu exprimée (l’hippocampe). Nos résultats confirment l’expression d’En1 et En2 dans l’hippocampe mature et décrivent les variations de l’expression de ces gènes au cours du développement de cette structure. En1 et En2 présentent des patrons d’expression différents pendant la première semaine postnatale et chez l’adulte suggérant que des variations du dosage génique d’Engrailed sont liées à certaines phases du développement, en particulier au début de la synaptogenèse. Nous avons également découvert que dans les cultures de cellules d’hippocampe Engrailed est exprimé dans les neurones et que son expression est plus forte dans les neurones GABA-ergiques, notamment dans leurs prolongements dendritiques et axonaux. Nous avons constaté qu’un excès d’Engrailed (décrit dans certains cas de TSA) augmente la complexité dendritique ainsi que la densité des épines dendritiques plastiques mais sans augmenter parallèlement la formation de synapses matures excitatrices. Nous avons observé des variations de densité des épines dendritiques chez les souris En2-/- et les souris En1+/-, ce qui confirme l’implication d’Engrailed dans leur formation ou leur stabilisation. Si dans nos conditions expérimentales l’excès d’Engrailed ne modifie pas la densité des synapses, un mutant d’Engrailed qui présente une interaction réduite avec eIF4E est moins efficace qu’Engrailed pour augmenter la densité des épines et diminue la densité des boutons présynaptiques et le synaptic matching. Ces résultats indiquent que l’interaction avec eIF4E régule au moins en partie les effets d’Engrailed sur la spinogenèse et suggèrent également une implication d’Engrailed dans la formation ou la stabilisation des boutons présynaptiques. Le rôle clef d’eIF4E dans la traduction permet de postuler que certains effets d’Engrailed observés dans notre étude pourraient dépendre de la synthèse protéique. Nos résultats montrent à cet égard qu’Engrailed augmente la synthèse protéique dans les neurones d’hippocampe. Cette traduction est différente de celle induite par la LTP chimique (LTPc) car insensible à l’action des oligomères synthétiques d’AβO, responsables sous leur forme naturelle de synaptopathies dans le contexte de la maladie d’Alzheimer. Engrailed permet également de restaurer la traduction défaillante de neurones issus de souris TG2576, modèles de la maladie d’Alzheimer. Dans leur ensemble, nos résultats identifient Engrailed comme un nouvel acteur de la plasticité dendritique. Ils révèlent qu’un excès d’Engrailed au cours de la synaptogenèse modifie les caractéristiques des dendrites, une situation susceptible d’altérer les caractéristiques fonctionnelles du réseau dendritique dans une situation de surexpression pathologique de la protéine. (...)<br>Engrailed (En) is an important transcription factor in embryo’s segmentation and anterior-posterior axis establishment during early embryogenesis. As several homeoproteins, Engrailed can act as an extracellular signalling molecule which can be internalized by target cells thanks to its penetratin domain and act through transcriptional and/or translation dependent mechanisms. Engrailed has for instance, translation-dependent effects on axonal guidance and cerebral infusion of Engrailed protects dopaminergic neurons in a Parkinson disease model by increasing mitochondrial protein translation. Also, cognitive defects were observed in En1+/+ and En2-/- and En2 expression is increased in ASD patients. This work consisted in extending the knowledge of Engrailed expression and functions. We explored the links with a telencephalic structure where it is a priori fewly expressed (hippocampus). Our results confirm En1 and En2 expression in the mature hippocampus and describe their respective expression along the development of this structure. En1 and En2 have different expression patterns during the first post-natal week as well as in the adulthood suggesting a genetic dosage of Engrailed during the development, specifically with the beginning of synaptogenesis. We also reveal that Engrailed, expressed in hippocampal neurons, is more expressed in GABA-ergic neurons, notably in their dendritic and axonal neurites. We observe that an excess of Engrailed (described in some ASD cases) increases dendritic complexity as well as plastic dendritic spine density, without affecting mature excitatory synapses. We show that En2-/- and heterozygote En1 mice have variations in dendritic spine density, which confirms that Engrailed is involved either in their formation or stabilization. Even though our experiments show no modification of synapse density with an excess of Engrailed, a mutant showing a decreased eIF4E interaction and less efficient than wild type Engrailed to increase dendritic spine density, decreases presynaptic button density and synaptic matching. Those results indicate that eIF4E interaction with Engrailed is, at least in part, responsible for its effects on spinogenesis and suggest a role of Engrailed in presynaptic button formation/stabilization. Key-role of eIF4E in translation allow to hypothesize that some of Engrailed effects we report could be translation dependent. In this sense, our results show that Engrailed is able to increase proteic synthesis in hippocampal neurons. This translation is different from the one induced by chemical LTP (LTPc): it is not altered by synthetic AβO, which are the main toxic agent when produced at abnormally high levels in Alzheimer disease. Engrailed is also able to restore defaulting translation in neurons from Alzheimer disease mice model (TG2576). As a whole, our results identify Engrailed as a novel actor in dendritic plasticity. They reveal that an excess of Engrailed during synaptogenesis can modify dendrite characteristics. This can lead to dendritic network dysfunction in a context of pathologic surexpression of Engrailed. Our observations open to new perspectives contributing to a better understanding of the relationship between Engrailed and ASD. Finally, this work lays the foundation to potentially fruitful links between Engrailed and AβOligomers signalling pathways, where modulation of protein synthesis could be a therapeutic lever in physiopathologic conditions
35
Rösch, Jan Harald. "Analysis of activity-dependent morphological plasticity of dendritic spines on hippocampal neurons." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-9914.
Full text
36
Cassenaer, Stijn Laurent Gilles Konishi Masakazu. "Spike-timing dependent plasticity and synchronous oscillations in an invertebrate olfactory system /." Diss., Pasadena, Calif. : California Institute of Technology, 2008. http://resolver.caltech.edu/CaltechETD:etd-12202007-160330.
Full text
37
Lee, Kevin Fu-Hsiang. "Dynamics of Synapse Function during Postnatal Development and Homeostatic Plasticity in Central Neurons." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32449.
Full textAbstract:
The majority of fast excitatory neurotransmission in the brain occurs at glutamatergic synapses. The extensive dendritic arborisations of pyramidal neurons in the neocortex and hippocampus harbor thousands of synaptic connections, each formed on tiny protrusions called dendritic spines. Spine synapses are rapidly established during early postnatal development – a key period in neural circuit assembly – and are subject to dynamic activity-dependent plasticity mechanisms that are believed to underlie neural information storage and processing for learning and memory. Recent decades have seen remarkable progress in identifying diverse plasticity mechanisms responsible for regulating synapse structure and function, and in understanding the processes underlying computation of synaptic inputs in the dendrites of individual neurons. These advances have strengthened our understanding of the biological mechanisms underlying brain function but, not surprisingly, they have also raised many new questions. Using a combination of whole-cell electrophysiology, 2-photon imaging and glutamate uncaging in rodent brain slice preparations, I have helped to document the subtype-specific regulation of glutamate receptors during a homeostatic form of synaptic plasticity at CA1 pyramidal neurons of the hippocampus, and have discovered novel synaptic calcium dynamics during a critical period of neural circuit formation. First, we found that during a homeostatic response to prolonged inactivity, both AMPA and NMDA subtypes of glutamate receptors undergo a switch in subunit composition at synapses, but exhibit a divergence in their subcellular localization at extrasynaptic regions of the plasma membrane (this work was published in the Journal of Neuroscience in 2013). In separate series of experiments using 2-photon calcium imaging, I discovered a functional coupling between NMDA receptor activation and intracellular calcium release at dendritic spines and dendrites that is selectively expressed during a critical period of synapse formation. This synaptic calcium signaling mechanism enabled the transformation of distinct spatiotemporal patterns of synaptic input into salient biochemical signals, and is thus apt to locally regulate synapse development along individual dendritic branches. Consistent with this hypothesis, I found evidence for non-random clustering of synapse development between neighboring dendritic spines. Together, these experimental results expand the current understanding of the dynamics of synapse function during homeostatic plasticity and early postnatal development.
---
Les synapses glutamatergiques soutiennent la majorité de la neurotransmission excitatrice rapide du cerveau. Des milliers de ces synapses, localisées sur de minuscules saillies appelées épines dendritiques, décorent les vastes arborisations dendritiques des neurones pyramidaux du néocortex et de l'hippocampe. Ces synapses sont formées tôt lors du développement postnatal et sont soumises à des mécanismes dynamiques de plasticité qui sous-tendent, croit-on, les capacités d'apprentissage et de mémoire du cerveau. Les dernières décennies ont vu des progrès remarquables dans l'identification de divers mécanismes de régulation de la structure et de la fonction des synapses sur différentes échelles de temps, et dans la compréhension des processus qui régissent l’intégration des inputs synaptiques au niveau des dendrites individuelles. Ces progrès ont renforcé notre compréhension des éléments fondamentaux régissant la fonction cérébrale et ont ouvert de nouvelles voies d’investigations neurophysiologiques. En utilisant une combinaison d’électrophysiologie cellulaire, d'imagerie à deux-photons et de photolibération de glutamate sur des neurones pyramidaux de la région CA1 de l'hippocampe de rats, j’ai contribué à la découverte et à la caractérisation de nouvelles régulations des récepteurs du glutamate durant la plasticité synaptique homéostatique. J’ai également découvert un nouveau type de dynamique de calcium synaptique relié à une organisation spatiale du développement des synapses pendant une période critique de l’ontogénie des circuits neuronaux. Dans la première étude, nous avons constaté que lors d'une plasticité de type homéostatique induite par une inactivité prolongée, les récepteurs de glutamate de types AMPA et NMDA sont soumis à un changement important dans la composition de leurs sous-unités. De plus, nous avons observé un ciblage différentiel de ces récepteurs vers des compartiments subcellulaires spécifiques des neurones. Dans une série d'expériences séparée utilisant l’imagerie calcique à deux-photons, j’ai découvert un couplage fonctionnel durant le développent entre l'activation des récepteurs NMDA et une libération de calcium intracellulaire qui envahit tant les épines dendritiques que les dendrites. J’ai également trouvé que ce mécanisme de signalisation de calcium synaptique transforme des motifs spatiotemporels d’activités synaptiques spécifiques en signaux biochimiques post-synaptiques de manière à potentiellement réguler l’organisation spatiale des synapses durant le développement. Conformément à cette hypothèse, j’ai observé des manifestations fonctionnelles claires de regroupement dans l’espace de synapses de forces similaires le long de branches dendritiques individuelles. Ensemble, ces résultats expérimentaux élargissent notre compréhension actuelle de de la fonction des synapses durant la plasticité homéostatique ainsi que durant le développement postnatal du cerveau. En étudiant les mécanismes neurophysiologiques de base, il sera possible d'avoir un aperçu plus profond du fonctionnement du cerveau et de ses pathologies.
38
Falez, Pierre. "Improving spiking neural networks trained with spike timing dependent plasticity for image recognition." Thesis, Lille 1, 2019. http://www.theses.fr/2019LIL1I101.
Full textAbstract:
La vision par ordinateur est un domaine stratégique, du fait du nombre potentiel d'applications avec un impact important sur la société. Ce secteur a rapidement progressé au cours de ces dernières années, notamment grâce aux avancées en intelligence artificielle et plus particulièrement l'avènement de l'apprentissage profond. Cependant, ces méthodes présentent deux défauts majeurs face au cerveau biologique : ils sont extrêmement énergivores et requièrent de gigantesques bases d'apprentissage étiquetées. Les réseaux de neurones à impulsions sont des modèles alternatifs qui permettent de répondre à la problématique de la consommation énergétique. Ces modèles ont la propriété de pouvoir être implémentés de manière très efficace sur du matériel, afin de créer des architectures très basse consommation. En contrepartie, ces modèles imposent certaines contraintes, comme l'utilisation uniquement de mémoire et de calcul locaux. Cette limitation empêche l'utilisation de méthodes d'apprentissage traditionnelles, telles que la rétro-propagation du gradient. La STDP est une règle d'apprentissage, observée dans la biologie, qui peut être utilisée dans les réseaux de neurones à impulsions. Cette règle renforce les synapses où des corrélations locales entre les temps d'impulsions sont détectées, et affaiblit les autres synapses. La nature locale et non-supervisée permet à la fois de respecter les contraintes des architectures neuromorphiques, et donc d'être implémentable de manière efficace, mais permet également de répondre aux problématiques d'étiquetage des bases d'apprentissage. Cependant, les réseaux de neurones à impulsions entraînés grâce à la STDP souffrent pour le moment de performances inférieures aux méthodes d'apprentissage profond. La littérature entourant la STDP utilise très majoritairement des données simples mais le comportement de cette règle n'a été que très peu étudié sur des données plus complexes, tel que sur des bases avec une variété d'images importante.L'objectif de ce manuscrit est d'étudier le comportement des modèles impulsionnels, entraîné via la STDP, sur des tâches de classification d'images. Le but principal est d'améliorer les performances de ces modèles, tout en respectant un maximum les contraintes imposées par les architectures neuromorphiques. Une première partie des contributions proposées dans ce manuscrit s'intéresse à la simulation logicielle des réseaux de neurones impulsionnels. L'implémentation matérielle étant un processus long et coûteux, l'utilisation de simulation est une bonne alternative pour étudier plus rapidement le comportement des différents modèles. La suite des contributions s'intéresse à la mise en place de réseaux impulsionnels multi-couches. Les réseaux composés d'un empilement de couches, tel que les méthodes d'apprentissage profond, permettent de traiter des données beaucoup plus complexes. Un des chapitres s'articule autour de la problématique de perte de fréquence observée dans les réseaux de neurones à impulsions. Ce problème empêche l'empilement de plusieurs couches de neurones impulsionnels. Une autre partie des contributions se concentre sur l'étude du comportement de la STDP sur des jeux de données plus complexes, tels que les images naturelles en couleur. Plusieurs mesures sont utilisées, telle que la cohérence des filtres ou la dispersion des activations, afin de mieux comprendre les raisons de l'écart de performances entre la STDP et les méthodes plus traditionnelles. Finalement, la réalisation de réseaux multi-couches est décrite dans la dernière partie des contributions. Pour ce faire, un nouveau mécanisme d'adaptation des seuils est introduit ainsi qu'un protocole permettant l'apprentissage multi-couches. Il est notamment démontré que de tels réseaux parviennent à améliorer l'état de l'art autour de la STDP<br>Computer vision is a strategic field, in consequence of its great number of potential applications which could have a high impact on society. This area has quickly improved over the last decades, especially thanks to the advances of artificial intelligence and more particularly thanks to the accession of deep learning. Nevertheless, these methods present two main drawbacks in contrast with biological brains: they are extremely energy intensive and they need large labeled training sets. Spiking neural networks are alternative models offering an answer to the energy consumption issue. One attribute of these models is that they can be implemented very efficiently on hardware, in order to build ultra low-power architectures. In return, these models impose certain limitations, such as the use of only local memory and computations. It prevents the use of traditional learning methods, for example the gradient back-propagation. STDP is a learning rule, observed in biology, which can be used in spiking neural networks. This rule reinforces the synapses in which local correlations of spike timing are detected. It also weakens the other synapses. The fact that it is local and unsupervised makes it possible to abide by the constraints of neuromorphic architectures, which means it can be implemented efficiently, but it also provides a solution to the data set labeling issue. However, spiking neural networks trained with the STDP rule are affected by lower performances in comparison to those following a deep learning process. The literature about STDP still uses simple data but the behavior of this rule has seldom been used with more complex data, such as sets made of a large variety of real-world images.The aim of this manuscript is to study the behavior of these spiking models, trained through the STDP rule, on image classification tasks. The main goal is to improve the performances of these models, while respecting as much as possible the constraints of neuromorphic architectures. The first contribution focuses on the software simulations of spiking neural networks. Hardware implementation being a long and costly process, using simulation is a good alternative in order to study more quickly the behavior of different models. Then, the contributions focus on the establishment of multi-layered spiking networks; networks made of several layers, such as those in deep learning methods, allow to process more complex data. One of the chapters revolves around the matter of frequency loss seen in several spiking neural networks. This issue prevents the stacking of multiple spiking layers. The center point then switches to a study of STDP behavior on more complex data, especially colored real-world image. Multiple measurements are used, such as the coherence of filters or the sparsity of activations, to better understand the reasons for the performance gap between STDP and the more traditional methods. Lastly, the manuscript describes the making of multi-layered networks. To this end, a new threshold adaptation mechanism is introduced, along with a multi-layer training protocol. It is proven that such networks can improve the state-of-the-art for STDP
39
Kwag, Jeehyun. "Synaptic control of spike timing and spike timing-dependent plasticity during theta frequency oscillation in hippocampal CA1 pyramidal neurons." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487275.
Full textAbstract:
Spike timing during oscillation has been suggested to play an important role in hippocampal processing. However, how the hippocampal network and the individual neurons interact to precisely control spike timing when they receive synaptic inputs from two major excitatory input pathways - Schaffer collateral and perforant path - during natural network oscillation is yet unknown. Investigation of spike timing control mechanism would shed light on how the local STDP learning rule could be influenced by different cortical inputs during theta oscillation. Here I used whole-cell path-clamp recording of CAl pyramidal neurons in vitro and dynamic clamp to simulate in vivo-like theta frequency oscillation at the soma to characterise the spike timing responses of CAl pyramidal neurons to Schaffer collateral and perforant path inputs during theta oscillation and present them as phase response curves (PRCs), Analysis of PRCs revealed that postsynaptic spike times could not only be advanced but also be delayed depending on the timing of excitatory inputs relative to the oscillation. Such control of spike timing during theta oscillation was dependent on the synaptic weight of the input and the frequency of the oscillation. Ih and GABAB receptor-mediated inhibition were identified as an intrinsic and synaptic mechanism, respectively, underlying spike time delay during oscillation. Activation of both Ih and GABAi3 receptor-mediated inhibition by perforant path stimulation contributed to greater spike time delay compared to that with Schaf.:fer collateral input stimulation which was only mediated by Ih. Such different spike timing characteristics were important in STDP induction at the Schaffer collateral-CAl pyramidal cell synapse, Depending on the timing of the perforant path activation during theta oscillation, perforant path input could control the timing of the postsynaptic spike during STDP induction which could reverse the sign of the synaptic modification, Thus, during natural network oscillation with multiple synaptic inputs active, timing of the heterosynaptic inputs from entorhinal cortex to the hippocampus could control the outcome of the homosynaptic plasticity in the CAL These results may have implications for how the external information could be encoded and stored in the hippocampal network.
40
Chevy, Quentin. "Rôle du transporteur neuronal Potassium/Chlore KCC2 dans la plasticité des synapses glutamatergiques." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066041/document.
Full textAbstract:
L'efficacité de la transmission synaptique GABAergique est influencée par la concentration intracellulaire en ions chlorure. Dans les neurones matures, l'extrusion de ces ions par le transporteur neuronal potassium chlore de type 2 (KCC2) permet l'influx d'ions chlorure lors de l'activation des récepteurs du GABA de type A. Néanmoins, KCC2 est aussi enrichi à proximité des synapses excitatrices portées par les épines dendritiques qui correspondent à des protrusions dendritiques enrichies en actine. Alors que l'effet d'une suppression de KCC2 sur l'homéostasie des ions chlorure et la transmission GABAergique est largement documenté, peu de choses sont connues sur l'impact qu'une telle suppression peut avoir sur la transmission glutamatergique. Lors de ma thèse, j'ai exploré le rôle de KCC2 dans la potentialisation à long terme (LTP) de la transmission glutamatergique à l'origine des phénomènes d'apprentissage et de mémorisation. Ce travail a révélé que la suppression de KCC2 compromet les modifications fonctionnelles et structurales sous-tendant la LTP. Cet effet est associé à une inhibition de la cofilin, protéine responsable de la dépolymérisation de l'actine, qui corrèle avec une augmentation de la quantité d'actine filamenteuse dans les épines dendritiques. En empêchant l'inhibition de la cofilin liée à l'absence de KCC2, il m'a alors été possible de restaurer la LTP suggérant que KCC2 pourrait influencer cette forme de plasticité en régulant la dynamique de polymérisation du cytosquelette d'actine. Mes résultats démontrent que la fonction de KCC2 va au-delà du contrôle de l'homéostasie des ions chlorure et influence les mécanismes de plasticité de la synapse excitatrice<br>The polarity and efficacy of GABAergic synaptic transmission are both influenced by the intra-neuronal chloride concentration. In mature neurons, chloride extrusion through the neuronal K/Cl cotransporter KCC2 allows an inhibitory influx of chloride upon activation of GABAA receptors. Nevertheless, KCC2 is enriched in the vicinity of excitatory synapses within the dendritic spines that are actin-rich protrusions emerging from dendritic shafts. While it has become clear that KCC2 suppression alters chloride homeostasis and GABA signaling, little is known on its impact on glutamatergic transmission. In the laboratory, we have previously demonstrated that KCC2 suppression in mature neurons leads to decreased glutamatergic transmission efficacy through an ion-transport independent function of KCC2. During my PhD, I have explored how KCC2 may also impact LTP of glutamatergic synapses. My work reveals that KCC2 suppression compromises both functional and structural LTP at these synapses. This effect is associated with inhibition of the actin-severing protein cofilin and enhanced mobilization of F-actin in dendritic spines. Since LTP can be rescued by preventing cofilin inhibition upon KCC2 suppression, I suggest KCC2 might influence LTP through altered actin cytoskeleton dynamics. My results demonstrate that KCC2 function extends beyond the mere control of neuronal chloride homoeostasis and suggest regulation of KCC2 membrane stability may act as a metaplastic switch to gate long term plasticity at excitatory synapses in cortical neurons
41
Ozturk, Ibrahim. "Learning spatio-temporal spike train encodings with ReSuMe, DelReSuMe, and Reward-modulated Spike-timing Dependent Plasticity in Spiking Neural Networks." Thesis, University of York, 2017. http://etheses.whiterose.ac.uk/21978/.
Full textAbstract:
SNNs are referred to as the third generation of ANNs. Inspired from biological observations and recent advances in neuroscience, proposed methods increase the power of SNNs. Today, the main challenge is to discover efficient plasticity rules for SNNs. Our research aims are to explore/extend computational models of plasticity. We make various achievements using ReSuMe, DelReSuMe, and R-STDP based on the fundamental plasticity of STDP. The information in SNNs is encoded in the patterns of firing activities. For biological plausibility, it is necessary to use multi-spike learning instead of single-spike. Therefore, we focus on encoding inputs/outputs using multiple spikes. ReSuMe is capable of generating desired patterns with multiple spikes. The trained neuron in ReSuMe can fire at desired times in response to spatio-temporal inputs. We propose alternative architecture for ReSuMe dealing with heterogeneous synapses. It is demonstrated that the proposed topology exactly mimic the ReSuMe. A novel extension of ReSuMe, called DelReSuMe, has better accuracy using less iteration by using multi-delay plasticity in addition to weight learning under noiseless and noisy conditions. The proposed heterogeneous topology is also used for DelReSuMe. Another plasticity extension based on STDP takes into account reward to modulate synaptic strength named R-STDP. We use dopamine-inspired STDP in SNNs to demonstrate improvements in mapping spatio-temporal patterns of spike trains with the multi-delay mechanism versus single connection. From the viewpoint of Machine Learning, Reinforcement Learning is outlined through a maze task in order to investigate the mechanisms of reward and eligibility trace which are the fundamental in R-STDP. To develop the approach we implement Temporal-Difference learning and novel knowledge-based RL techniques on the maze task. We develop rule extractions which are combined with RL and wall follower algorithms. We demonstrate the improvements on the exploration efficiency of TD learning for maze navigation tasks.
42
Humble, James. "Learning, self-organisation and homeostasis in spiking neuron networks using spike-timing dependent plasticity." Thesis, University of Plymouth, 2013. http://hdl.handle.net/10026.1/1499.
Full textAbstract:
Spike-timing dependent plasticity is a learning mechanism used extensively within neural modelling. The learning rule has been shown to allow a neuron to find the onset of a spatio-temporal pattern repeated among its afferents. In this thesis, the first question addressed is ‘what does this neuron learn?’ With a spiking neuron model and linear prediction, evidence is adduced that the neuron learns two components: (1) the level of average background activity and (2) specific spike times of a pattern. Taking advantage of these findings, a network is developed that can train recognisers for longer spatio-temporal input signals using spike-timing dependent plasticity. Using a number of neurons that are mutually connected by plastic synapses and subject to a global winner-takes-all mechanism, chains of neurons can form where each neuron is selective to a different segment of a repeating input pattern, and the neurons are feedforwardly connected in such a way that both the correct stimulus and the firing of the previous neurons are required in order to activate the next neuron in the chain. This is akin to a simple class of finite state automata. Following this, a novel resource-based STDP learning rule is introduced. The learning rule has several advantages over typical implementations of STDP and results in synaptic statistics which match favourably with those observed experimentally. For example, synaptic weight distributions and the presence of silent synapses match experimental data.
43
Albers, Christian [Verfasser], Klaus [Akademischer Betreuer] Pawelzik, and Stefan [Akademischer Betreuer] Bornholdt. "Functional Implications of Synaptic Spike Timing Dependent Plasticity and Anti-Hebbian Membrane Potential Dependent Plasticity / Christian Albers. Gutachter: Klaus Pawelzik ; Stefan Bornholdt. Betreuer: Klaus Pawelzik." Bremen : Staats- und Universitätsbibliothek Bremen, 2015. http://d-nb.info/107560947X/34.
Full text
44
Hauser, Florian [Verfasser]. "Formation and stability of spiking cell assemblies with spike-timing-dependent synaptic plasticity / Florian Hauser." Ulm : Universität Ulm. Fakultät für Ingenieurwissenschaften und Informatik, 2012. http://d-nb.info/1028567995/34.
Full text
45
Iglesias, Javier. "Emergence of oriented circuits driven by synaptic pruning associated with spike-timing-dependent plasticity (STDP)." Université Joseph Fourier (Grenoble), 2005. https://tel.archives-ouvertes.fr/tel-00010650.
Full textAbstract:
L'élagage massif des synapses après une croissance excessive est une phase normale de la maturation du cerveau des mammifères. L'élagage commence peu avant la naissance et est complété avant l'âge de la maturité sexuelle. Les facteurs déclenchants capables d'induire l'élagage des synapses pourraient être liés à des processus dynamiques qui dépendent de la temporalité relative des potentiels d'actions. La plasticité synaptique à modulation temporelle relative STDP correspond à un changement de la force synaptique basé sur l'ordre des décharges pré- et post-synaptiques. La relation entre l'efficacité synaptique et l'élagage des synapses suggère que les synapses les plus faibles pourraient être modifiées et retirées au moyen d'une règle "d'apprentissage" faisant intervenir une compétition. Cette règle de plasticité pourrait produire le renforcement des connections parmi les neurones qui appartiennent à une assemblée de cellules caractérisée par des motifs de décharge récurrents. A l'inverse, les connections non activées de façon récurrente pourraient voir leur efficacité diminuée et être finalement éliminées. Le but principal de notre travail est de déterminer dans quelles conditions de telles assemblées pourraient émerger d'un réseau d'unités integrate-and-fire connectées aléatoirement à la surface d'une grille bidimensionnelle recevant à la fois du bruit et des entrées organisées dans les dimensions temporelle et spatiale. L'originalité de notre étude tient dans la taille relativement grande du réseau, 10'000 unités, dans la durée des simulations, 1 million d'unités de temps, et dans l'utilisation d'une règle STDP originale compatible avec une implémentation matérielle<br>Massive synaptic pruning following over-growth is a general feature of mammalian brain maturation. Pruning starts near time of birth and is completed by time of sexual maturation. Trigger signals able to induce synaptic pruning could be related to dynamic functions that depend on the timing of action potentials. Spike-timing-dependent synaptic plasticity (STDP) is a change in the synaptic strength based on the ordering of pre, and postsynaptic spikes. The relation between synaptic efficacy and synaptic pruning suggests that the weak synapses may be modified and removed through competitive "learning" rules. This plasticity rule might produce the strengthening of the connections among neurons that belong to cell assemblies characterized by recurrent patterns of firing. Conversely, the connections that are not recurrently activated might decrease in efficiency and eventually be eliminated. The main goal of our study is to determine whether or not, and under which conditions, such cell assemblies may emerge out of a locally connected random network of integrate-and-fire units distributed on a 2D lattice receiving background noise and content-related input organized in both temporal and spatial dimensions. The originality of our study stands on the relatively large size of the network, 10,000 units, the duration of the experiment, 1,000,000 time units (one time unit corresponding to the duration of a spike), and the application of an original bio-inspired STDP modification rule compatible with hardware implementation
46
Mittmann, Wolfgang Matthias Oliver. "Spike output and synaptic plasticity in a feed-forward inhibitory microcircuit in the cerebellar cortex." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1446252/.
Full textAbstract:
Feed-forward inhibitory circuits are common building blocks in the mammalian brain and lead to excitatory input also activating inhibitory input to a common postsynaptic neuron. Such circuits are important for regulating neuronal excitability and timing of activity in the brain. In this thesis I have explored the mechanisms and consequences of feed-forward inhibition in the rat cerebellar cortex, which is known to be involved in coordination and timing of movement. Voltage clamp recordings from Purkinje cells in cerebellar slices exhibit a biphasic current waveform in response to stimulation of parallel fibres, consisting of an excitatory postsynaptic current (EPSC) followed by an inhibitory postsynaptic current (IPSC). The latency difference between the two components - only 1.4 ms - and the complete block of the biphasic response by glutamate receptor antagonists confirmed the second component as feed forward inhibition (FFI). The rapid onset of FFI shortens EPSPs, which enhances spike precision and limits summation of independent inputs. Next, I showed that the latency of FFI does not change with distance along active parallel fibres. This suggests that desynchronisation of action potentials travelling along the parallel fibres is insufficient to cause feed-forward inhibition to arrive ahead of excitation, a theory previously used to explain the observed lack of 'beams' of active Purkinje cells along the parallel fibres. Instead, it is argued that this may result from spatial or temporal spread of activity in the granule cell layer leading to early arrival of inhibition. Both excitation and inhibition in Purkinje cells are subject to plastic changes induced by climbing fibre activation. In a feed-forward network, what is the net effect of this plasticity on the output of the cerebellar cortex First I showed that both inhibition and excitation undergo long-term depression (LTD) to a similar extent when paired with climbing fibre input. This plasticity was reflected in corresponding changes in Purkinje cell spike output triggered by independent inhibitory and excitatory inputs: parallel fibre LTD reduced, and LTD of inhibition increased the number of spikes evoked by the respective inputs. To examine the net effect of simultaneous plasticity of inhibition and excitation on Purkinje cell output with a feed-forward input, I simulated synaptic inputs with dynamic clamp and systematically changed the ratio of excitation and inhibition as well as the amplitude of both components. Depressing both components as observed when pairing the isolated components with the climbing fibre, reduced spike output for feed-forward inputs with small inhibitory components, while for inputs with stronger inhibition the spike output increased. Finally, I showed that pauses after spike bursts evoked by strong parallel fibre inputs in the absence of inhibition scaled with input strength. A classical climbing fibre LTD protocol reduced these pauses, which thus encode information stored by synaptic plasticity for downstream neurons. These findings are discussed in the context of classical theories of cerebellar learning, which are concluded to require revision or refinement.
47
Piochon, Claire. "NMDA receptors in cerebellar Purkinje cells : development and synaptic plasticity in the mouse." Paris 6, 2008. https://tel.archives-ouvertes.fr/tel-00378780.
Full textAbstract:
Structure cérébrale nécessaire à la coordination motrice et aux apprentissages moteurs, ainsi qu’à certaines tâches cognitives, le cervelet est aussi un pertinent modèle d’étude du fonctionnement des neurones. Elément clef de la fonction cérébelleuse, la cellule de Purkinje reçoit et intègre de nombreux signaux excitateurs glutamatergiques. De manière surprenante, le récepteur du glutamate N-methyl-D-aspartate (R-NMDA), qui joue un rôle clé dans la plupart des neurones intégrateurs du cerveau, a gardé une fonction méconnue dans les cellules de Purkinje néonatales, et sa présence est demeurée quasiment inconnue chez les cellules adultes. Cette thèse propose un rôle des R-NMDA dans l’effet neuroprotecteur de la dépolarisation, lors de la mort cellulaire développementale des cellules de Purkinje néonatales. D’autre part, cette thèse clarifie la présence de R-NMDA chez la cellule de Purkinje de la souris adulte. Elle montre également leur rôle dans la plasticité synaptique ainsi que dans la stabilisation sélective des connections synaptiques.
48
Bennett, James Edward Matthew. "Pattern formation in neural circuits by the interaction of travelling waves with spike-timing dependent plasticity." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:29387080-4213-4179-98b6-bf3d4c49dd00.
Full textAbstract:
Spontaneous travelling waves of neuronal activity are a prominent feature throughout the developing brain and have been shown to be essential for achieving normal function, but the mechanism of their action on post-synaptic connections remains unknown. A well-known and widespread mechanism for altering synaptic strengths is spike-timing dependent plasticity (STDP), whereby the temporal relationship between the pre- and post-synaptic spikes determines whether a synapse is strengthened or weakened. Here, I answer the theoretical question of how these two phenomenon interact: what types of connectivity patterns can emerge when travelling waves drive a downstream area that implements STDP, and what are the critical features of the waves and the plasticity rules that shape these patterns? I then demonstrate how the theory can be applied to the development of the visual system, where retinal waves are hypothesised to play a role in the refinement of downstream connections. My major findings are as follows. (1) Mathematically, STDP translates the correlated activity of travelling waves into coherent patterns of synaptic connectivity; it maps the spatiotemporal structure in waves into a spatial pattern of synaptic strengths, building periodic structures into feedforward circuits. This is analogous to pattern formation in reaction diffusion systems. The theory reveals a role for the wave speed and time scale of the STDP rule in determining the spatial frequency of the connectivity pattern. (2) Simulations verify the theory and extend it from one-dimensional to two-dimensional cases, and from simplified linear wavefronts to more complex realistic and noisy wave patterns. (3) With appropriate constraints, these pattern formation abilities can be harnessed to explain a wide range of developmental phenomena, including how receptive fields (RFs) in the visual system are refined in size and topography and how simple-cell and direction selective RFs can develop. The theory is applied to the visual system here but generalises across different brain areas and STDP rules. The theory makes several predictions that are testable using existing experimental paradigms.
49
Deroche, Marion. "Etudes optogénétique et pharmacologique de la connectivité et de la plasticité endocannabinoïde des synapses glutamatergiques du noyau accumbens de souris." Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0086.
Full textAbstract:
Le noyau accumbens (NAc) intègre des informations cognitives et affectives. Bien que le rôle du NAc dans les troubles neuropsychiatriques soit bien connu, une compréhension détaillée de ses circuits dans des conditions physiologiques fait défaut. Les neurones moyens épineux (MSNs) du NAc sont des neurones de projection GABAergiques qui expriment des récepteurs D1 ou D2. Ils reçoivent et intègrent des signaux glutamatergiques provenant notamment du cortex préfrontal (PFC), de l'hippocampe ventral (vHipp) et de l'amygdale basolatérale (BLA).Dans cette thèse, nous avons combiné des méthodes optogénétique et électrophysiologique pour dresser un portrait fonctionnel des synapses excitatrices sur les MSNs D1 et D2 dans le NAc de souris adulte. Nous avons observé que les MSNs D1 sont plus excitables que les D2. Ensuite, les propriétés synaptiques de vHipp, de la BLA et du PFC ont révélé une hiérarchie des afférences dépendant de l’identité des MSNs et de l’inhibition «feedforward». Nous avons constaté que la BLA est la voie dominante sur les MSNs D1, tandis que le PFC domine sur les D2. De plus, nous avons testé l’hypothèse que le système endocannabinoïde confère aux circuits excitateurs une plasticité spécifique des voies et des cellules. Ainsi, alors que les récepteurs CB1 dépriment uniformément les voies quelle que soit l’identité des MSNs, les récepteurs TRPV1 contrôlent les afférences de manière bidirectionnelle sur le NAc. Enfin, nous avons clarifié comment l'interaction des récepteurs TRPV1/CB1 façonne la plasticité au niveau des synapses identifiées de BLA-NAc. Ensemble, ces données révèlent un haut degré de spécificité des synapses et du circuit dans le NAc adulte<br>The nucleus accumbens (NAc) plays a key role in action selection by integrating cognitive and affective information. The NAc is implicated in numerous neuropsychiatric disorders, however a complete understanding of its circuits and their regulation in physiological conditions is missing. The principal cell type in the NAc, medium-spiny neurons MSNs are GABAergic projection neurons that express either D1 or D2 receptors. They receive and integrate glutamatergic inputs most notably from the prefrontal cortex (PFC), ventral hippocampus (vHipp) and basolateral amygdala (BLA).We combined optogenetic and electrophysiological methods to draw a functional portrait of excitatory disambiguated synapses onto D1 and D2 MSNs in the adult mouse NAc core. We first observed that adult D1- are inherently more excitable than D2-MSNs. Next, the synaptic properties of vHipp, BLA and PFC inputs revealed a hierarchy of synaptic inputs dependent on the identity of the postsynaptic target MSN and on circuit specific feedforward inhibition. We found that the BLA is the dominant excitatory pathway onto D1- while PFC inputs dominate D2-MSNs. Additionally, we tested the hypothesis that the endocannabinoid system endows excitatory circuits with pathway- and cell-specific plasticity. Thus, while CB1 receptors (CB1R) uniformly depress excitatory pathways irrespective of MSNs’ identity, TRPV1 receptors (TRPV1R) bidirectionally control inputs onto the NAc core in a pathway- and cell- specific manner. Finally, we clarified how the interplay of TRPV1R/CB1R shapes plasticity at identified BLA-NAc synapses. Together these data reveal a high degree of synapse and circuit specificity in the adult NAc core
50
Nakamura, Yasuko. "PICK1 mediates the structural plasticity of dendritic spines via the inhibition of Arp2/3-mediated actin polymerisation." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.525461.
Full text