Bibliografias temáticas / Balance locale Excitation/Inhibition

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Literatura científica selecionada sobre o tema "Balance locale Excitation/Inhibition"

Autor: Grafiati

Publicado: 14 de dezembro de 2024

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Artigos de revistas sobre o assunto "Balance locale Excitation/Inhibition"

Nguyen, Bao N., Allison M. McKendrick e Algis J. Vingrys. "Abnormal inhibition-excitation imbalance in migraine". Cephalalgia 36, n.º 1 (18 de março de 2015): 5–14. http://dx.doi.org/10.1177/0333102415576725.

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Background People with migraine show increased surround suppression of perceived contrast, a perceptual analogue of centre-surround antagonistic interactions in visual cortex. A proposed mechanism is that cortical ‘hyperexcitability’ or ‘hyperresponsivity’, a prominent theory in the migraine literature, drives abnormal excitatory-inhibitory balance to give increased local inhibition. The purpose of this cross-sectional study was to determine whether cortical hyperresponsivity and excitatory-inhibitory imbalance manifests in the visual cortical response of migraine sufferers. Methods Interictal steady-state visual evoked potentials (VEPs) in response to 0 to 97% contrast were recorded in 30 migraine participants (15 without aura, 15 with aura) and 21 non-headache controls. Monotonicity indices were calculated to determine response saturation or supersaturation. Contrast gain was modelled with a modified saturating hyperbolic function to allow for variation in excitation and inhibition. Results A greater proportion of migraine participants (43%) than controls (14%) exhibited significant VEP supersaturation at high contrast, based on monotonicity index (chi-square, p = 0.028). Supersaturation was also evident by the trend for greater suppressive exponent values in migraine compared to control individuals (Mann-Whitney rank sum, p = 0.075). Conclusions Supersaturation in migraine is consistent with excess excitation (hyperresponsivity) driving increased network inhibition and provides support for excitatory-inhibitory imbalance as a pathophysiological disturbance in migraine.

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Hamaguchi, Kosuke, Alexa Riehle e Nicolas Brunel. "Estimating Network Parameters From Combined Dynamics of Firing Rate and Irregularity of Single Neurons". Journal of Neurophysiology 105, n.º 1 (janeiro de 2011): 487–500. http://dx.doi.org/10.1152/jn.00858.2009.

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High firing irregularity is a hallmark of cortical neurons in vivo, and modeling studies suggest a balance of excitation and inhibition is necessary to explain this high irregularity. Such a balance must be generated, at least partly, from local interconnected networks of excitatory and inhibitory neurons, but the details of the local network structure are largely unknown. The dynamics of the neural activity depends on the local network structure; this in turn suggests the possibility of estimating network structure from the dynamics of the firing statistics. Here we report a new method to estimate properties of the local cortical network from the instantaneous firing rate and irregularity (CV2) under the assumption that recorded neurons are a part of a randomly connected sparse network. The firing irregularity, measured in monkey motor cortex, exhibits two features; many neurons show relatively stable firing irregularity in time and across different task conditions; the time-averaged CV2 is widely distributed from quasi-regular to irregular (CV2 = 0.3–1.0). For each recorded neuron, we estimate the three parameters of a local network [balance of local excitation-inhibition, number of recurrent connections per neuron, and excitatory postsynaptic potential (EPSP) size] that best describe the dynamics of the measured firing rates and irregularities. Our analysis shows that optimal parameter sets form a two-dimensional manifold in the three-dimensional parameter space that is confined for most of the neurons to the inhibition-dominated region. High irregularity neurons tend to be more strongly connected to the local network, either in terms of larger EPSP and inhibitory PSP size or larger number of recurrent connections, compared with the low irregularity neurons, for a given excitatory/inhibitory balance. Incorporating either synaptic short-term depression or conductance-based synapses leads many low CV2 neurons to move to the excitation-dominated region as well as to an increase of EPSP size.

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Brunel, Nicolas, e Xiao-Jing Wang. "What Determines the Frequency of Fast Network Oscillations With Irregular Neural Discharges? I. Synaptic Dynamics and Excitation-Inhibition Balance". Journal of Neurophysiology 90, n.º 1 (julho de 2003): 415–30. http://dx.doi.org/10.1152/jn.01095.2002.

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When the local field potential of a cortical network displays coherent fast oscillations (∼40-Hz gamma or ∼200-Hz sharp-wave ripples), the spike trains of constituent neurons are typically irregular and sparse. The dichotomy between rhythmic local field and stochastic spike trains presents a challenge to the theory of brain rhythms in the framework of coupled oscillators. Previous studies have shown that when noise is large and recurrent inhibition is strong, a coherent network rhythm can be generated while single neurons fire intermittently at low rates compared to the frequency of the oscillation. However, these studies used too simplified synaptic kinetics to allow quantitative predictions of the population rhythmic frequency. Here we show how to derive quantitatively the coherent oscillation frequency for a randomly connected network of leaky integrate-and-fire neurons with realistic synaptic parameters. In a noise-dominated interneuronal network, the oscillation frequency depends much more on the shortest synaptic time constants (delay and rise time) than on the longer synaptic decay time, and ∼200-Hz frequency can be realized with synaptic time constants taken from slice data. In a network composed of both interneurons and excitatory cells, the rhythmogenesis is a compromise between two scenarios: the fast purely interneuronal mechanism, and the slower feedback mechanism (relying on the excitatory-inhibitory loop). The properties of the rhythm are determined essentially by the ratio of time scales of excitatory and inhibitory currents and by the balance between the mean recurrent excitation and inhibition. Faster excitation than inhibition, or a higher excitation/inhibition ratio, favors the feedback loop and a much slower oscillation (typically in the gamma range).

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Wang, Jiang, Ruixue Han, Xilei Wei, Yingmei Qin, Haitao Yu e Bin Deng. "Weak signal detection and propagation in diluted feed-forward neural network with recurrent excitation and inhibition". International Journal of Modern Physics B 30, n.º 02 (20 de janeiro de 2016): 1550253. http://dx.doi.org/10.1142/s0217979215502537.

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Reliable signal propagation across distributed brain areas provides the basis for neural circuit function. Modeling studies on cortical circuits have shown that multilayered feed-forward networks (FFNs), if strongly and/or densely connected, can enable robust signal propagation. However, cortical networks are typically neither densely connected nor have strong synapses. This paper investigates under which conditions spiking activity can be propagated reliably across diluted FFNs. Extending previous works, we model each layer as a recurrent sub-network constituting both excitatory (E) and inhibitory (I) neurons and consider the effect of interactions between local excitation and inhibition on signal propagation. It is shown that elevation of cellular excitation–inhibition (EI) balance in the local sub-networks (layers) softens the requirement for dense/strong anatomical connections and thereby promotes weak signal propagation in weakly connected networks. By means of iterated maps, we show how elevated local excitability state compensates for the decreased gain of synchrony transfer function that is due to sparse long-range connectivity. Finally, we report that modulations of EI balance and background activity provide a mechanism for selectively gating and routing neural signal. Our results highlight the essential role of intrinsic network states in neural computation.

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Harris, Kameron Decker, Tatiana Dashevskiy, Joshua Mendoza, Alfredo J. Garcia, Jan-Marino Ramirez e Eric Shea-Brown. "Different roles for inhibition in the rhythm-generating respiratory network". Journal of Neurophysiology 118, n.º 4 (1 de outubro de 2017): 2070–88. http://dx.doi.org/10.1152/jn.00174.2017.

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Unraveling the interplay of excitation and inhibition within rhythm-generating networks remains a fundamental issue in neuroscience. We use a biophysical model to investigate the different roles of local and long-range inhibition in the respiratory network, a key component of which is the pre-Bötzinger complex inspiratory microcircuit. Increasing inhibition within the microcircuit results in a limited number of out-of-phase neurons before rhythmicity and synchrony degenerate. Thus unstructured local inhibition is destabilizing and cannot support the generation of more than one rhythm. A two-phase rhythm requires restructuring the network into two microcircuits coupled by long-range inhibition in the manner of a half-center. In this context, inhibition leads to greater stability of the two out-of-phase rhythms. We support our computational results with in vitro recordings from mouse pre-Bötzinger complex. Partial excitation block leads to increased rhythmic variability, but this recovers after blockade of inhibition. Our results support the idea that local inhibition in the pre-Bötzinger complex is present to allow for descending control of synchrony or robustness to adverse conditions like hypoxia. We conclude that the balance of inhibition and excitation determines the stability of rhythmogenesis, but with opposite roles within and between areas. These different inhibitory roles may apply to a variety of rhythmic behaviors that emerge in widespread pattern-generating circuits of the nervous system. NEW & NOTEWORTHY The roles of inhibition within the pre-Bötzinger complex (preBötC) are a matter of debate. Using a combination of modeling and experiment, we demonstrate that inhibition affects synchrony, period variability, and overall frequency of the preBötC and coupled rhythmogenic networks. This work expands our understanding of ubiquitous motor and cognitive oscillatory networks.

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Anticevic, Alan, e John Lisman. "How Can Global Alteration of Excitation/Inhibition Balance Lead to the Local Dysfunctions That Underlie Schizophrenia?" Biological Psychiatry 81, n.º 10 (maio de 2017): 818–20. http://dx.doi.org/10.1016/j.biopsych.2016.12.006.

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Vattikonda, Anirudh, Bapi Raju Surampudi, Arpan Banerjee, Gustavo Deco e Dipanjan Roy. "Does the regulation of local excitation–inhibition balance aid in recovery of functional connectivity? A computational account". NeuroImage 136 (agosto de 2016): 57–67. http://dx.doi.org/10.1016/j.neuroimage.2016.05.002.

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Esser, Steve K., Sean Hill e Giulio Tononi. "Breakdown of Effective Connectivity During Slow Wave Sleep: Investigating the Mechanism Underlying a Cortical Gate Using Large-Scale Modeling". Journal of Neurophysiology 102, n.º 4 (outubro de 2009): 2096–111. http://dx.doi.org/10.1152/jn.00059.2009.

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Effective connectivity between cortical areas decreases during slow wave sleep. This decline can be observed in the reduced interareal propagation of activity evoked either directly in cortex by transcranial magnetic stimulation (TMS) or by sensory stimulation. We present here a large-scale model of the thalamocortical system that is capable of reproducing these experimental observations. This model was constructed according to a large number of physiological and anatomical constraints and includes over 30,000 spiking neurons interconnected by more than 5 million synaptic connections and organized into three cortical areas. By simulating the different effects of arousal promoting neuromodulators, the model can produce a waking or a slow wave sleep-like mode. In this work, we also seek to explain why intercortical signal transmission decreases in slow wave sleep. The traditional explanation for reduced brain responses during this state, a thalamic gate, cannot account for the reduced propagation between cortical areas. Therefore we propose that a cortical gate is responsible for this diminished intercortical propagation. We used our model to test three candidate mechanisms that might produce a cortical gate during slow wave sleep: a propensity to enter a local down state following perturbation, which blocks the propagation of activity to other areas, increases in potassium channel conductance that reduce neuronal responsiveness, and a shift in the balance of synaptic excitation and inhibition toward inhibition, which decreases network responses to perturbation. Of these mechanisms, we find that only a shift in the balance of synaptic excitation and inhibition can account for the observed in vivo response to direct cortical perturbation as well as many features of spontaneous sleep.

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Linster, Christiane, e Claudine Masson. "A Neural Model of Olfactory Sensory Memory in the Honeybee's Antennal Lobe". Neural Computation 8, n.º 1 (janeiro de 1996): 94–114. http://dx.doi.org/10.1162/neco.1996.8.1.94.

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We present a neural model for olfactory sensory memory in the honeybee's antennal lobe. To investigate the neural mechanisms underlying odor discrimination and memorization, we exploit a variety of morphological, physiological, and behavioral data. The model allows us to study the computational capacities of the known neural circuitry, and to interpret under a new light experimental data on the cellular as well as on the neuronal assembly level. We propose a scheme for memorization of the neural activity pattern after stimulus offset by changing the local balance between excitation and inhibition. This modulation is achieved by changing the intrinsic parameters of local inhibitory neurons or synapses.

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Busche, Marc Aurel, e Arthur Konnerth. "Impairments of neural circuit function in Alzheimer's disease". Philosophical Transactions of the Royal Society B: Biological Sciences 371, n.º 1700 (5 de agosto de 2016): 20150429. http://dx.doi.org/10.1098/rstb.2015.0429.

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An essential feature of Alzheimer's disease (AD) is the accumulation of amyloid-β (Aβ) peptides in the brain, many years to decades before the onset of overt cognitive symptoms. We suggest that during this very extended early phase of the disease, soluble Aβ oligomers and amyloid plaques alter the function of local neuronal circuits and large-scale networks by disrupting the balance of synaptic excitation and inhibition ( E / I balance) in the brain. The analysis of mouse models of AD revealed that an Aβ-induced change of the E / I balance caused hyperactivity in cortical and hippocampal neurons, a breakdown of slow-wave oscillations, as well as network hypersynchrony. Remarkably, hyperactivity of hippocampal neurons precedes amyloid plaque formation, suggesting that hyperactivity is one of the earliest dysfunctions in the pathophysiological cascade initiated by abnormal Aβ accumulation. Therapeutics that correct the E / I balance in early AD may prevent neuronal dysfunction, widespread cell loss and cognitive impairments associated with later stages of the disease. This article is part of the themed issue ‘Evolution brings Ca 2+ and ATP together to control life and death’.

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Teses / dissertações sobre o assunto "Balance locale Excitation/Inhibition"

Vallet, Anais. "Etude de la balance Excitatiοn/Ιnhibitiοn de régiοns cérébrales impliquées dans une tâche de cοntrôle inhibiteur : mοdélisatiοn de dοnnées οbtenues en Ιmagerie par Résοnance Μagnétique fοnctiοnnelle et inversiοn". Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMC014.

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En psychologie, le contrôle inhibiteur est un mécanisme cognitif qui permet de stopper une ré-ponse motrice, émotionnelle ou cognitive non adaptée pour la réalisation d’un but désiré. Au niveaucérébral, le contrôle inhibiteur est associé au fonctionnement en réseau de régions cérébrales, quipeut être mesuré à partir du signal BOLD en IRMf. Des régions de contrôle préfrontales abaissentl’activité BOLD de régions cibles. L’IRMf permet de mesurer de manière indirecte l’activité desneurones. Comment peut-on alors inférer à partir de données d’IRMf des propriétés excitatriceset inhibitrices (E/I) neurales au sein de régions cérébrales impliquées dans une tâche de contrôleinhibiteur ?Nous partons d’un modèle biophysique non linéaire, hiérarchique qui décrit les évolutions tempo-relles des activités neurales excitatrice et inhibitrice par région (Naskar et al., 2021). Ces varia-tions d’activité produisent des changements BOLD dans chaque région cérébrale. L’analyse de cemodèle nous permet de : 1) identifier des paramètres neuraux de la balance E/I ; 2) montrer quel’augmentation d’activité BOLD d’une région de contrôle ne permet pas d’abaisser l’activité BOLDd’une région cible parce que les régions sont connectées par leurs neurones excitateurs uniquement ;3) proposer une nouvelle architecture de connectivité pour le permettre ; 4) étudier comment labaisse d’activité de la région cible dépend de la balance E/I dans la cible. Nous proposons alorsune nouvelle procédure d’inversion. Nous en vérifions la fiabilité avec des simulations, avant deprésenter une preuve de concept sur les données d’un sujet pendant une tâche de Think/NoThink,un paradigme d’étude du contrôle inhibiteur des intrusions mnésiques (Mary et al., 2020)
In psychology, inhibitory control is a cognitive mechanism that stops a motor, emotional orcognitive response from achieving a desired goal. At cerebral level, inhibitory control is associatedwith a network of brain regions, whose function may be measured using BOLD signals from fMRI.Prefrontal control regions lower the BOLD activity of target regions. fMRI provides an indirectmeasure of the activity of neurons. How can we then infer from fMRI data, neural excitatory andinhibitory (E/I) properties of brain regions involved in an inhibitory control task ?We start with a non-linear biophysical model that describes by region the temporal evolutionof neural excitatory and inhibitory activities (Naskar et al., 2021). These variations in activityproduce BOLD changes in each brain region. Analysis of this model enables us to : 1) identifyneural parameters of the E/I balance ; 2) show that increasing the BOLD activity of a controlregion does not lower the BOLD activity of a target region, since these regions are connected bytheir excitatory neurons only ; 3) propose a new connectivity architecture to enable this ; 4) studyhow the lowering of activity in the target region depends on the E/I balance in the target region.We then propose a new inversion procedure. We check its reliability through simulations, beforepresenting a proof-of-concept using real data from a subject during a Think/No-Think task, aparadigm used for studying the inhibitory control of memory intrusions (Mary et al., 2020)

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Luo, Jingjing. "Modelling evoked local field potentials : an investigation into balanced synaptic excitation and inhibition". Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/6143/.

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Buscher, Nathalie. "Cognition and the balance of excitation and inhibition in mouse cortico-limbic circuits". Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.690894.

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The medial prefrontal cortex (mPFC} and hippocampus (HPC} are central to executive control, spatial learning and working memory. In order to enable behavioral control, the function of the mPFC and HPC is tuned by complex interplay between excitatory (glutamatergic) and inhibitory (GABAergic) neurotransmitter systems. This thesis has employed lesions, pharmacological and optogenetic methodologies to investigate how the relationship between excitation and inhibition within the adult mouse mPFC and HPC affects cognition, using a battery of touchscreen-based operant assays: the automated spatial array task (ASAT), Spatial Reversal (SR) and Visual Discrimination (VD). Behavioral testing following excitotoxic lesions showed that the HPC was strongly implicated in the performance of both spatial tests (ASAT and SR), while removal of the mPFC had only marginal effects on learning with several trends that did not reach significance. Additionally, in VD, effects were only present as trends towards an involvement of the mPFC in formations of new stimulus-reward relationships. Interdependent processing spanning the mPFC and HPC while not directly assessed can be considered likely to explain complex changes in task performance. Using the described assays helped validate their application to test mPFC and HPC function in mice.

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Amar, Muriel. "Etude de la balance Excitation / Inhibition des neurones pyramidaux du cortex visuel de rat". Habilitation à diriger des recherches, Université Paris Sud - Paris XI, 2009. http://tel.archives-ouvertes.fr/tel-00367158.

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Les travaux de l'équipe sont centrés sur la régulation de l'excitabilité et de la plasticité des réseaux neuronaux. La modulation de l'intégration synaptique est étudiée au niveau cortical où il s'agit de déterminer quels sont les acteurs de la plasticité homéostatique et comment l'action spécifique de certains types de récepteurs (cholinergique, sérotoninergique) peut moduler la balance excitation/inhibition déterminée dans des neurones pyramidaux de couche 5 qui génèrent les signaux de sortie du cortex visuel.

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Petrash, Hilary A. "Maintaining the Balance: Coordinating Excitation and Inhibition in a Simple Motor Circuit: A Dissertation". eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/633.

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The generation of complex behaviors often requires the coordinated activity of diverse sets of neural circuits in the brain. Activation of neuronal circuits drives behavior. Inappropriate signaling can contribute to cognitive disorders such as epilepsy, Parkinson’s, and addiction (Nordberg et al., 1992; Quik and McIntosh, 2006; Steinlein et al., 2012). The molecular mechanisms by which the activity of neural circuits is coordinated remain unclear. What are the molecules that regulate the timing of neural circuit activation and how is signaling between various neural circuits achieved? While much work has attempted to address these points, answers to these questions have been difficult to ascertain, in part owing to the diversity of molecules involved and the complex connectivity patterns of neural circuits in the mammalian brain. My thesis work addresses these questions in the context of the nervous system of an invertebrate model organism, the nematode Caenorhabditis elegans. The locomotory circuit contains two subsets of motor neurons, excitatory and inhibitory, and the body wall muscle. Dyadic synapses from excitatory neurons coordinate the simultaneous activation of inhibitory neurons and body wall muscle. Here I identify a distinct class of ionotropic acetylcholine receptors (ACR-12R) that are expressed in GABA neurons and contain the subunit ACR-12. ACR-12R localize to synapses of GABA neurons and facilitate consistent body bend amplitude across consecutive body bends. ACR-12Rs regulate GABA neuron activity under conditions of elevated ACh release. This is in contrast to the diffuse and modulatory role of ACR-12 containing receptors expressed in cholinergic motor neurons (ACR-2R) (Barbagallo et al., 2010; Jospin et al., 2009). Additionally, I show transgenic animals expressing ACR-12 with a mutation in the second transmembrane domain [ACR-12(V/S)] results in spontaneous contractions. Unexpectedly, I found expression of ACR-12 (V/S) results in the preferential toxicity of GABA neurons. Interestingly loss of presynaptic GABA neurons did not have any obvious effects on inhibitory NMJ receptor localization. Together, my thesis work demonstrates the diverse roles of nicotinic acetylcholine receptors (nAChRs) in the regulation of neuronal activity that underlies nematode movement. The findings presented here are broadly applicable to the mechanisms of cholinergic signaling in vertebrate models.

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Chen, Xi. "Design and optimization of small peptides that regulate the balance of synaptic excitation and inhibition". Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/61467.

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The balance of synaptic excitation and inhibition plays a very important role in maintaining the function of central nervous system (CNS) and the imbalance is involved in neurologic diseases such as autism and epilepsy. PSD95 and gephyrin have been studied as scaffolding proteins, having critical functional and structural roles in excitatory and inhibitory synapses, respectively. In the thesis, I have attempted to develop small systemically applicable peptides that can reversibly knock down PSD95 or gephyrin in vitro and in vivo, using the novel peptide-mediated technology recently developed in our lab, as tools for modulating the balance of synaptic excitation and inhibition. The efficacy of the peptides knocking down respective targeted proteins was tested by immunoblots after the cultured neurons were treated with the peptides for the desired time at various concentrations. I found that peptides that target either PSD95 or gephyrin showed toxicity to the neurons in a dose and time dependent manner utilizing the LDH assay. The toxicity may also contribute to the reduction of protein levels. Using one of the peptides, TAT-NR2B9C-CMA that targets PSD95 as example, I systemically investigated the causes of the toxicity and tested several strategies to reduce the toxicity while keeping the efficacy of the protein knockdown. I found that while multiple treatments at low dose could not successfully separate the cell death and knockdown effect, treatment at high doses with shortened durations appeared partially effective in reducing the toxicity and maintaining knockdown efficacy. However, this protocol may not be applicable in vivo. I next modified the intrinsic properties of peptides by shortening CMA targeting motifs and/or adding a linker between the binding sequences and CMA targeting motif. I found that while both strategies could decrease the toxicity with varied degree, peptides with short CMA targeting motif kept the knockdown efficacy. Taken together, my study demonstrated the effective strategies to reduce the toxicity of the peptides one can consider in the process of developing novel protein knockdown peptides as novel research tools and therapeutic reagents.
Medicine, Faculty of
Graduate

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Pracucci, Enrico. "Unraveling alterations of excitation/inhibition balance in in vivo models of epilepsy and genetic autism". Doctoral thesis, Scuola Normale Superiore, 2019. http://hdl.handle.net/11384/85883.

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One prominent feature of brain computation is the excitation inhibition balance (E/I balance) that represents one of the main homeostatic functions of the brain. Its aim is to maintain the neural circuits in a narrow and safe range of action. Within this range, the brain network can receive and analyze sensory inputs and produce a modulated output, proportional to the stimuli intensity. Any imbalance in this equilibrium leads to abnormal responses to external stimuli and results in pathological behavior. Indeed, neurological pathologies known for featuring a deep alteration of the E‐I balance are epilepsy and autism, which often occur together in the same patient. Several human genetic syndromes caused by alterations of genes involved in neural development feature signs like autism and epilepsy. Thus, they represent important cases for studying and understanding the role of these single altered genes in the development and regulation of the brain balance. In return, we hope that this knowledge of these genes and more generally of human brain network can be useful in treating the patients affected by these conditions and can help us improve their quality of life. In my work, I studied the regulation of the E/I balance in mouse models of neurological diseases from three different points of view. In the first set of experiments, I studied the E/I balance in a focal model of epileptiform activity. This model is produced by the local application of bicuculline to the mouse cortex. Bicuculline is a competitive GABAA receptor antagonist that, when applied, leads to the development of persistent and periodic interictal spikes at the injection site, while activity appears to be normal in nearby areas that are not reached by bicuculline. In our experiments, we showed that, even in the apparently normal area, there is a disruption of cortical computation. Specifically, the disruption occurs whenever an interictal spike is generated in the epileptic focus. This can have important impact on our understanding of epilepsy and of its treatment since interictal spikes are a common feature not only of epileptic patients, but can also appear in non‐epileptic subject, apparently without any consequence. From our results, we concluded that interictal activity can actually interfere with brain operation not only in the center of the epileptiform activity, but also in the connected areas, where the E/I balance is not directly disrupted. These results provide an example of the fact that apparently non‐symptomatic interictal spikes can affect brain computation. The second experimental model that I studied is a mouse model for a specific human genetic disease: the Phelan‐McDermid syndrome. This is a developmental disease, caused by a genomic deletion at site 22q13. The main suspect for causing the disease is one gene, Shank3, which encodes for a scaffold protein localized in the post‐synaptic density of glutamatergic synapses. In this model, we studied the computation of visual stimuli and we found an alteration of the contrast‐response curve. This is a defining relationship of visual processing: it is the transfer function that converts the visual input into a neural output. This means that to each intensity of visual stimulation corresponds a certain intensity of the neural response, of the visual cortex. We determined that, in Shank3 mutant mice, this curve was altered and showed an increased response to less intense stimuli and showed also a poor modulation of responses to high‐contrast stimulations. An interpretation of this can be that these mice are more sensitive to low‐contrast stimuli, but completely lose the ability of telling apart different high‐contrast stimuli from each other. Therefore, the Phelan McDermid mouse becomes “blinded” by weak stimulations as if they were seeing strong stimulus. Finally, we studied the behavior of the chloride ion in a drug‐induced epileptic seizure model. Chloride ion is of pivotal importance in neurons were the activation of ionotropic GABA and glycine receptors, which increase chloride membrane conductance in response to GABA or glycine release respectively. The intracellular concentration of chloride ions decides what is the effect of GABA release. Traditionally, ionotropic GABA receptors activation was thought to be inhibitory only, but the excitatory or inhibitory nature of these receptors is determined by the intracellular concentration of chloride ions. This concentration in normal adult neurons is thought to be around 5 mM: at this concentration, the effect of the activation of GABA receptors is an inhibition of the postsynaptic element. We investigated if the chloride concentration can be varied under extreme pathologic conditions as during epileptic seizures in a drug induced mouse model. In these animals, the epileptic seizures were produced by local administration of 4‐aminopyridine (4‐AP), a potassium channel antagonist. The effect of 4‐AP is to cause accumulation of chloride ions in neurons and this suggests that, in epileptic crisis, the role of inhibitory neurons can actually favor excitation.

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Reynolds, Charlene Helen. "Changes in the balance of excitation and inhibition in the human motor cortex with voluntary movements". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0024/MQ40813.pdf.

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Leonzino, M. "NEURONAL MORPHOLOGY AND EXCITATION/INHIBITION BALANCE IN A MOUSE MODEL OF AUTISM: CORRELATION WITH BEHAVIORAL PHENOTYPES". Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/229412.

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The role of oxytocin (OXT) in controlling social behavior suggests a link to neuropsychiatric conditions in which social behavior behavior is aberrant or even absent, such as autism. Mice lacking the OXT receptor (Oxtr-/-) display an autistic-like phenotype, including deficits in social interaction, impaired cognitive flexibility (murine correlates of autism core symptoms), increased aggression and susceptibility to seizure (common co-occurring conditions). The deficit in cognitive flexibility is particularly interesting, because it is present in few animal model of autism. For this reason we decided to investigate its underlying neurobiological and molecular mechanisms. First, we compared Oxtr+/+and Oxtr-/- neuronal morphology and spine remodeling following a cognitive behavioral test. Interestingly, we highlighted, in the Oxtr-/- mice, an enhanced connectivity and overuse of the dorsolateral striatum, possibly arising from an hippocampal dysfunction, and we proposed it as substrate for habit-like symptoms and cognitive rigidity. Second, we investigated, at the molecular level, possible sources of this hippocampal dysfunction. In particular, we analyzed Oxtr-/- hippocampal neurons for the expression of proteins involved in the setting and maintenance of excitatio-inhibition (E-I) balance. We found an upregulation of several inwardly-rectifying K+ channels (belonging to Kir2 and Kir3 families), which could alter membrane excitability, and a lack of the physiological upregulation of the chloride transporter KCC2 during development, that may lead to aberrant GABAergic signaling in mature neurons. These data give important indications that the E-I balance is altered at multiple levels in Oxtr-/- hippocampal neurons, as an altered ratio between Glutamatergic and GABAergic synapses was also previously observed in these cultures. These observations are particularly intriguing, because an E-I imbalance has been frequently associated with several neurodevelopmental disorders such as autism. Third, we disclosed an OXTR-mediated pathway modulating KCC2 expression that may restore a correct E-I balance in hippocampal neurons. All this information could be useful to understand the pathophysiology of cognitive rigidity and to develop new therapies addressing specific symptoms of autism.

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Moreau, Alexandre. "Neuromodulation des réseaux neuronaux : contrôle sérotoninergique de la balance excitation-inhibition dans le cortex visuel de rat". Phd thesis, Université Paris Sud - Paris XI, 2009. http://tel.archives-ouvertes.fr/tel-00441514.

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Le traitement de l'information sensorielle par le cortex cérébral requiert l'activation harmonieuse de micro-circuits neuronaux excitateurs et inhibiteurs interconnectés, ciblant les neurones pyramidaux de couche 5. Ces derniers élaborent les signaux de sortie corticaux et reçoivent un ratio de 20% d'excitation (E) et 80% d'inhibition (I). La dérégulation de cette balance E-I ou du système sérotoninergique conduit à des neuropathologies telles la dépression et la schizophrénie mais les interrelations entre la sérotonine et la balance E-I sont inconnues. Nous avons montré que la 5-HT endogène module la balance E-I en fonction du type de récepteur 5-HT recruté (1A, 2A, 3, 4, 7) et de sa localisation spécifique dans la colonne corticale. Ces données électrophysiologiques constituent la première évidence pour une action modulatrice fine de la sérotonine corticale sur la balance E-I et révèle la ségrégation fonctionnelle des récepteurs 5-HT dans les réseaux de neurones sensoriels.

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Livros sobre o assunto "Balance locale Excitation/Inhibition"

Reynolds, Charlene Helen. Changes in the balance of excitation and inhibition in the human motor cortex with voluntary cortex. Ottawa: National Library of Canada, 1998.

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Capítulos de livros sobre o assunto "Balance locale Excitation/Inhibition"

McCormick, David A., You-Sheng Shu e Andrea Hasenstaub. "Balanced Recurrent Excitation and Inhibition in Local Cortical Networks". In Excitatory-Inhibitory Balance, 113–24. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0039-1_8.

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Okun, Michael, e Ilan Lampl. "Balance of Excitation and Inhibition". In Scholarpedia of Touch, 577–90. Paris: Atlantis Press, 2015. http://dx.doi.org/10.2991/978-94-6239-133-8_44.

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Galarreta, Mario, e Shaul Hestrin. "Fast Spiking Cells and the Balance of Excitation and Inhibition in the Neocortex". In Excitatory-Inhibitory Balance, 173–85. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0039-1_11.

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van Vreeswijk, C., e H. Sompolinsky. "Irregular Firing in Cortical Circuits with Inhibition/Excitation Balance". In Computational Neuroscience, 209–13. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9800-5_34.

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Sakamoto, Kazuhiro, Naohiro Saito, Shun Yoshida e Hajime Mushiake. "Excitation-Inhibition Balance of Prefrontal Neurons During the Execution of a Path-Planning Task". In Advances in Cognitive Neurodynamics (IV), 547–52. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9548-7_79.

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Garg, Akhil R., Basabi Bhaumik e Klaus Obermayer. "The Balance Between Excitation and Inhibition Not Only Leads to Variable Discharge of Cortical Neurons but Also to Contrast Invariant Orientation Tuning". In Neural Information Processing, 90–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-30499-9_13.

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Benarroch, Eduardo E. "Peripheral and Spinal Mechanisms of Nociception". In Neuroscience for Clinicians, editado por Eduardo E. Benarroch, 655–73. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0035.

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Pain is a conscious subjective experience driven by activity of nociceptors. Pain includes not only nociception but also abnormal transmission and processing of painful stimuli. Nociception involves unmyelinated and small myelinated fibers from small dorsal root ganglion neurons that respond to noxious heat, mechanical, or chemically stimuli. These neurons are functional and biochemically heterogeneous in terms of their sensitivity to stimuli, type of afferent axons, neurochemical composition, and targets in the dorsal horn. They activate both second-order projection neurons and different subsets of excitatory and inhibitory interneurons that have a major role in processing of sensory information. Mutations affecting ion channels in nociceptors, inflammatory mediators, or peripheral nerve injury trigger changes and expression of ion channels and receptors. This results in increased excitability of nociceptors, known as peripheral sensitization. Abnormal activity in nociceptors triggers plastic channels in the dorsal horn resulting in altered balance between excitation and inhibition, resulting in central sensitization. Local activation of microglia and astrocytes plays a major role in this process. Elucidation of mechanisms of peripheral and central sensitization provide insight into the pathophysiology of neuropathic pain and potential therapeutic targets for its treatment.

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Murphy, Allison J., e Farran Briggs. "Structure and Function of Corticothalamic Pathways of Layer 6 Neurons". In The Cerebral Cortex and Thalamus, editado por Francisco Clasca e Sonja B. Hofer, 143–51. Oxford University PressNew York, 2023. http://dx.doi.org/10.1093/med/9780197676158.003.0014.

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Abstract Throughout the brain, corticothalamic (CT) neurons project from layer 6 of the cerebral cortex to various regions of the thalamus, including first-order thalamic nuclei that receive input from the sensory periphery and higher-order thalamic nuclei that derive their inputs mainly from cortical areas. Layer 6 CT neurons are diverse in terms of their cellular morphology and physiological properties, and they likely subserve a number of heterogeneous functions. While the number of synapses originating from layer 6 CT neurons onto thalamic cells is large, their terminals are distally located, small in size, and produce small, facilitating excitatory postsynaptic potentials, all characteristics that define these synaptic interactions as “modulatory” rather than “driving.” Importantly, layer 6 CT circuits often include axon collaterals that target inhibitory neuronal populations within the thalamus, enabling CT feedback to dynamically regulate the balance of excitation and inhibition among thalamic neurons. Although much is yet to be learned about the function of layer 6 CT feedback in the thalamus, current evidence from sensory systems suggests that CT feedback can shape the tuning properties of thalamic neurons as well as influence the timing and precision with which thalamic cells encode incoming sensory information. Other functions of layer 6 CT feedback include regulating arousal state, attention, and sleep. Overall, layer 6 CT pathways provide diverse inputs to thalamus that are likely critical for multiple aspects of brain function.

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Lőrincz, Magor L., Vincenzo Crunelli e Francois David. "Excitation-Inhibition Balance in Absence Seizure Ictogenesis". In Jasper's Basic Mechanisms of the Epilepsies, editado por Massimo Avoli, Marco de Curtis, Christophe Bernard e Ivan Soltesz, 389–400. 5^a ed. Oxford University PressNew York, 2024. http://dx.doi.org/10.1093/med/9780197549469.003.0020.

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Abstract Thirty percent of children with absence seizures are pharmaco-resistant, and 60% suffer from neuropsychiatric comorbidities that often persist even after full pharmacological control of the seizures. This highlights the need for a detailed comprehension of the cellular and network mechanisms of these nonconvulsive seizures. Generally, network hyperexcitability and hypersynchrony underlying seizure ictogenesis are thought to originate from impaired inhibition or enhanced excitation. In absence seizures, there is a markedly enhanced synchrony in cortico-thalamic and cortico-basal ganglia-thalamic networks, but solid evidence from genetic animal models indicates that at the single-cell and neuronal population levels GABAergic inhibition is generally increased while excitation is mostly either unchanged or decreased. Here, recent results on intrinsic conductances and network mechanisms within cortico-thalamic and cortico-basal ganglia-thalamic circuits are highlighted that support this view.

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Staley, Kevin J. "Ionic Mechanisms of Ictogenic Disinhibition". In Jasper's Basic Mechanisms of the Epilepsies, editado por Michael A. Rogawski, 1467–88. 5^a ed. Oxford University PressNew York, 2024. http://dx.doi.org/10.1093/med/9780197549469.003.0071.

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Abstract Seizures are a consequence of an imbalance between excitation and inhibition. Of course, most of the time the brain does not generate seizure activity, even in severely epileptic patients. So there must be a way for the balance of excitation and inhibition to shift to engender seizure activity. Here two types of shifts are considered. The first is a temporal shift in the efficacy of inhibition. The neurotransmitter GABA, released from interneurons and acting on postsynaptic GABAA receptors, is the principal mechanism of synaptic inhibition in the brain. The GABAA receptor is unique in that it gates an anionic membrane current that can change direction under both physiological and pathological circumstances. Some of the pathological shifts can lead to seizure activity. The second shift in the efficacy of inhibition is anatomical. Some GABAA synapses that were meant to gate anion flow in the inhibitory direction instead gate anion flux in the opposite direction. This can occur as a consequence of either dysgenesis or the effects of injury and recovery from injury. This chapter reviews the basis for the direction of GABAA currents, and then discusses how they can be altered in time and space to increase the probability of seizure activity. Finally, therapeutic interventions are discussed.

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Trabalhos de conferências sobre o assunto "Balance locale Excitation/Inhibition"

Zaqout, Sami, Lena-Luise Becker, Ayman Mustafa, Nadine Krame, Ulf Strauss e Angela M. Kaindl. "Role of Cdk5rap2 in neocortical inhibition and excitation balance". In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0117.

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Autosomal recessive primary microcephaly type 3 (MCPH3) is characterized by congenital microcephaly and intellectual disability. Further features include hyperactivity and seizures. The disease is caused by biallelic mutations in the Cyclin-dependent kinase 5 regulatory subunit-associated protein 2 gene CDK5RAP2. In the mouse, Cdk5rap2 mutations similarly result in reduced brain size and a strikingly thin neocortex already at early stages of neurogenesis that persists through adulthood. The microcephaly phenotype in MCPH arises from a neural stem cell proliferation defect. Here, we report a novel role for Cdk5rap2 in the regulation of dendritic development and synaptogenesis of neocortical layer 2/3 pyramidal neurons using a combined morphological and electrophysiological approach

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Cosa Klein, P., U. Ettinger, M. Schirner, P. Ritter, P. Falka, N. Koutsouleris e J. Kambeitz. "Brain network simulations indicate effect of neuregulin-1 genotype on excitation-inhibition balance in cortical dynamics". In Abstracts of the 2nd Symposium of the Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP) and Deutsche Gesellschaft für Biologische Psychiatrie (DGBP). Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3403020.

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Ponzi, Adam. "Model of Balance of Excitation and Inhibition in Hippocampal Sharp Wave Replays and Application to Spatial Remapping". In 2007 International Joint Conference on Neural Networks. IEEE, 2007. http://dx.doi.org/10.1109/ijcnn.2007.4371329.

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Vechkapova, S. O., e A. L. Proskura. "THE CONTRIBUTION OF LEPTIN AND INSULIN TO THE REGULATION OF THE DENSITY OF SYNAPTIC AMPA RECEPTORS IN THE HIPPOCAMPUS". In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-304.

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In these theses we consider the molecular mechanisms of the insulin and leptin receptor signaling pathways involved in the regulation of the density of synaptic AMPA receptors in the CA1 field of the hippocampus. The proposed reconstruction of molecular events makes it possible to evaluate the contributions of insulin and leptin to synaptic plasticity and maintaining the balance of excitation and inhibition in the neural networks of the hippocampus during the implementation of higher cognitive functions.

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