Relevant bibliographies by topics / Neuroplasticity

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Neuroplasticity'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Neuroplasticity"

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Németh, Viktor. "Neuroplasticity." Belügyi Szemle 69, no. 6. ksz. (December 1, 2021): 124–27. http://dx.doi.org/10.38146/bsz.spec.2021.6.8.

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As editor Bruce Tidor sets it in the preface of the book, published in the volume of the MIT Essential Knowledge series: ‘Synthesizing specialized subject matter for non-specialists and engaging critical topics through fundamentals, each of these compact volumes offers readers a point of access to complex ideas.’ (Costandi, 2016). In this book of the series Moheb Costandi provides the reader with a celar and coherent picture about neuroplasticity and neurogenesis . Not just at the level of theories and research results, but also regarding various stages of practical application. It is equally applicable for average people in areas of everyday life- adult education, lifelong learning, and mental training, too. Costandi’s book is decidedly good background material for Anders Hansen’s practical book ‘The Real Happy Pill: Power Up Your Brain by Moving Your Body’ (Németh, 2020).
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Thompson, Cynthia K. "Neuroplasticity." Journal of Communication Disorders 33, no. 4 (July 2000): 357–66. http://dx.doi.org/10.1016/s0021-9924(00)00031-9.

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Spitzer, M. "Neuroplasticity." European Psychiatry 17 (May 2002): 12. http://dx.doi.org/10.1016/s0924-9338(02)80053-0.

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de Oliveira, Rúbia Maria Weffort. "Neuroplasticity." Journal of Chemical Neuroanatomy 108 (October 2020): 101822. http://dx.doi.org/10.1016/j.jchemneu.2020.101822.

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Lenn, Nicholas J. "Neuroplasticity." Infants & Young Children 3, no. 3 (January 1991): 39–48. http://dx.doi.org/10.1097/00001163-199101000-00007.

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Damulin, I. V. Damulin. "MALADAPTIVE NEUROPLASTICITY." Pharmateca 10_2018 (October 19, 2018): 6–10. http://dx.doi.org/10.18565/pharmateca.2018.10.6-10.

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Lawtoo, Nidesh. "Conrad’s Neuroplasticity." Modernism/modernity 23, no. 4 (2016): 771–88. http://dx.doi.org/10.1353/mod.2016.0073.

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Naryshkin, A. G., I. V. Galanin, and A. Yu Egorov. "Controlled Neuroplasticity." Human Physiology 46, no. 2 (March 2020): 216–23. http://dx.doi.org/10.1134/s0362119720020103.

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Larsen, Deborah S. "Why Neuroplasticity?" Journal of Neurologic Physical Therapy 36, no. 2 (June 2012): 110–11. http://dx.doi.org/10.1097/npt.0b013e3182567076.

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Morley, J. S. "Central neuroplasticity." Pain 54, no. 3 (September 1993): 363–64. http://dx.doi.org/10.1016/0304-3959(93)90042-n.

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Dissertations / Theses on the topic "Neuroplasticity"

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Abrahamsson, Sebastian. "Neuroplasticity induced by exercise." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-13909.

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As opposed to earlier beliefs, the brain is altering itself throughout an individual’s life. The process of functional or structural alterations is referred to as plasticity, and can be induced by several factors such as experience or physical exercise. In this thesis, the research area of experience-dependent plasticity, with focus on exercise-induced plasticity is examined critically. Evidence from a vast array of studies are reviewed and compared in order to find whether physical exercise can induce neural plasticity in the human brain, how it may be beneficial, and what some of the plausible mediators of exercise-induced plasticity are. The findings demonstrated in this thesis suggest that although there are knowledge gaps and limitations in the literature, physical exercise can indeed result in exhibited plasticity as well as being beneficial for the human brain in several ways.
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Watt, William C. "Neuroplasticity in olfactory sensation /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/6252.

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Rossi, Sonja. "Neuroplasticity of word learning." Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19420.

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Das Wortlernen begleitet unser Leben von der Kindheit bis ins Alter. Kleinkinder lernen ihre Muttersprache(n), aber auch Erwachsene lernen neue Wörter, z.B. beim Fremdspracherwerb. Unter gewissen Umständen muss eine neue Sprache wieder erlernen werden, wie z.B. nach einer Gehirnläsion. Wie meistert unser Gehirn diese herausfordernden Wortlernsituationen? Um die Neuroplastizität des Wortlernens zu untersuchen, wurden unterschiedliche neurowissenschaftliche Methoden (Elektroenzephalographie, funktionelle Nahinfrarotspektroskopie, voxel-basierte Läsion-Verhalten/EEG Mapping), teilweise in Kombination, bei Kleinkindern, Kindern und Erwachsenen sowie Patienten mit einer Gehirnläsion im Vergleich zu älteren Kontrollprobanden angewendet. 5 Experimente untersuchten die neuronale Verarbeitung von Pseudowörtern, welche mutter- und fremdsprachlichen phonotaktischen Regeln (d.h. die Kombination von verschiedenen Phonemen) folgten, in unterschiedlichen Lernsettings bei monolingualen Teilnehmern. Gesunde Erwachsene aber auch 6monatige und ältere Teilnehmer und Patienten konnten diese Regeln differenzieren. Beteiligte Gehirnareale umfassten ein links-hemisphärisches fronto-temporales Netzwerk. Die Verarbeitung universeller Spracheigenschaften, andererseits, zeigte sich in parietalen Regionen. Während Erwachsene eine klare Dominanz der linken Hemisphäre aufwiesen, nutzten 6monatige noch beide Gehirnhälften. Unterschiedliche Sprachtrainings (semantische Trainings oder Passives Zuhören) an drei aufeinanderfolgenden Tagen veränderten auch die Gehirnaktivität der Kleinkinder und der Erwachsenen und wiesen auf eine erhöhte Lernflexibilität hin. Im 6. Experiment lernten 5jährige bilinguale Kinder anhand pragmatischer Eigenschaften neue Adjektive und zeigten effizientere neuronale Mechanismen als Monolinguale. Die Ergebnisse unterstreichen die Wichtigkeit multi-methodologischer Ansätze, um genauere Einblicke in die komplexen Mechanismen der Neuroplastizität zu erlangen.
Word learning accompanies our everyday life from infancy to advanced age. Infants have to learn the native language(s) but also during adulthood word learning can take place, for example if we learn a new foreign language. Sometimes people are confronted with a situation in which they have to re-learn a language because of a brain lesion. How does the brain master these challenging word learning settings? To assess neuroplasticity of word learning several neuroscientific methods (electroencephalography, functional near-infrared spectroscopy, voxel-based lesion-behavior/EEG mapping), partially in combination, were used in infants, children, and adults as well as in patients suffering from a brain lesion compared to matched elderly controls. In 5 experiments neuronal processing of pseudowords corresponding to native and non-native phonotactic rules (i.e., the combination of different phonemes) was investigated under different learning conditions in monolingual participants. Healthy adults but also 6-month-old infants and elderly subjects and patients were able to differentiate these rules. Involved brain areas included a left-hemispheric network of fronto-temporal regions. When processing universal linguistic features, however, more parietal regions were involved. While adults revealed a clear left-dominant network, 6-month-olds still recruited bilateral brain areas. Differential language trainings (semantic or passive listening trainings) over three consecutive days also modulated brain activation in both infants and adults suggesting a high flexibility for learning native and non-native linguistic regularities. In a 6th experiment, bilingual 5-year-old children learned novel adjectives by means of pragmatic cues and revealed more efficient neuronal mechanisms compared to monolingual children. Findings underline the importance of multi-methodological approaches to get clearer insights into the complex machinery of neuroplasticity.
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Voss, Oliver Paul. "AMPA receptor potentiators : mechanisms of neuroplasticity." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/25276.

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The AMPA receptor potentiator LY404187 is able to significantly increase the average length of neuritic processes in the neuroblastoma cell line SH-SY5Y only in the presence of s-AMPA, and this response is dependent on AMPA receptor activation. The compound also increases neurofilament protein levels as well as levels of the BDNF receptor Trk-B. The increase in neuritic length is blocked by addition of an antibody specific for BDNF indicating that this neurotrophin is required for the induction of neurite growth. The ability to induce morphological change in neuronal processes of the compound was then tested in a rodent model of lesions and sprouting. Unilateral ibotenic lesions of the entorhinal cortex in mice produce a progressive and substantial loss of synapses in the molecular layer of the dentate gyrus. Twice daily s.c. injections of LY404187 for 14 and 28 days post-lesion did not produce any significant change in synaptophysin immunoreactivity in the dentate gyrus. There was also no change in the volume of the lesion in the entorhinal cortex. In a secondary study the rate of neurogenesis in the dentate gyrus was also measured. Administration of LY404187 failed to induce a change in the number of BrdU +ve cells within the sub-granular zone of the dentate gyrus. Any long term structural of behavioural change caused by prolonged AMPA receptor potentiation is likely to be underpinned by changes in protein expression. The levels of key proteins involved in the intracellular response to AMPA receptor activation were measured by Western Blot and immunohistochemistry and levels of the neurotransmitters dopamine and serotonin were measured by HPLC. The effect of chronic administration to the AMPA receptor potentiator LY450108 on the rate of neurogenesis and the development of newly born neuron in the hippocampus was also investigated.
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Habekost, Bonne. "Neuroplasticity induced by peripheral nerve stimulation." Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/3062.

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Non-invasive methods have been developed to induce plastic changes in the sensorimotor cortex. These rely on stimulating pairs of afferent nerves. By associative stimulation (AS) of two afferent nerves, excitability changes in the motor cortex occur as indicated by studies reporting changes in motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS). Repetitive stimulation of those nerves has a potential in rehabilitation and treatment of neurological disorders like stroke or spinal cord injury. Despite promising results and applications in human subjects using these methods, little is understood about the underlying basis for the changes which are seen. In the present study, behavioural, electrophysiological and immunohistochemical assessments were performed before and after paired associative and non-associative (NAS) median and ulnar nerve stimulation. Two macaque monkeys were trained to perform a skilled finger abduction task using refined behavioural methods. Monkeys were not able to move their thumb and index finger as selectively after one hour of paired AS as indicated by an increased number of errors and decreased performance measures. NAS however decreased error numbers and led to increased performances. Additionally, I recorded from identified pyramidal tract neurons and unidentified cells in primary motor cortex (M1), in two macaque monkeys before and after one hour of AS (and NAS) of the median and ulnar nerve. Cell discharge was recorded in response to electrical stimulation of each nerve independently. Some cells in M1 showed changed firing rates in response to nerve stimulation after AS (and NAS). Subsequently, structural changes in response to one week of paired AS were investigated. The laminar-specific density of parvalbumin-positive interneurons, perineuronal nets and the colocalisation of these two entities changed on the stimulated (in comparison to the non-stimulated) sensorimotor cortex. These findings suggest that the sensorimotor cortex undergoes plastic changes in response to AS (and NAS).
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Teo, J. T. H. "Motor learning and neuroplasticity in humans." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/17592/.

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The central nervous system is plastic, in that the number and strength of synaptic connections changes over time. In the adult the most important driver of such changes is experience, in the form of learning and memory. There are thought to be a number of rules, operating relatively local to each synapse that govern changes in strength and organisation. Some of these such as Hebbian plasticity or plasticity following repeated activation of a connection have been studied in detail in animal preparations. However, recent work with non-invasive methods of transcranial stimulation in human, such as transcranial magnetic stimulation, has opened the opportunity to study similar effects in the conscious human brain. In this thesis I use these methods to explore some of the presumed changes in synaptic connectivity in the motor cortex during different forms of motor learning. The experiments only concern learning in the healthy brain; however it seems likely that the same processes will be relevant to neurorehabilitation and disease of the nervous system. This thesis explores the link between neuroplasticity and motor learning in humans using non-invasive brain stimulation, pharmacological agents and psychomotor testing in 6 related studies. 1) Chapter 3 reports initial pharmacological investigations to confirm the idea that some of the long term effects of TMS are likely to involve LTP-like mechanisms. The study shows that NMDA agonism can affect the response to a repetitive form of TMS known as theta burst stimulation (TBS) 2) Following up on the initial evidence for the role of NMDA receptors in the long term effects of TBS, Chapter 4 explores the possible modulatory effects of dopaminergic drugs on TBS. 3) Chapter 5 takes the investigations to normal behaviours by examining how the NMDA dependent plasticity produced by TBS interacts with learning a simple motor task of rapid thumb abduction. The unexpected results force a careful examination of the possible mechanisms of motor learning in this task. 4) Chapter 6 expands on these effects by employing a battery of TMS methods as well as drug agents to examine the role of different intracortical circuits in ballistic motor learning. 5) Chapter 7 studies the plasticity of intracortical circuits involved in transcallosal inhibition. 6) Chapter 8 studies the interaction between synaptic plasticity invoked by TBS and sequence learning. The studies described in the thesis contribute to understanding of how motor learning and neuroplasticity interact, and possible strategies to enhance these phenomena for clinical application.
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Tisch, S. H. D. "Neuroplasticity following pallidal stimulation for dystonia." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445124/.

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Dystonia is a disabling condition characterised by involuntary muscle spasms and abnormal postures. Its pathophysiology is incompletely understood but most lines of evidence point to an underlying defect of basal ganglia function leading to abnormal corticomotor output. Various abnormalities have been shown, including abnormal neuronal activity in basal ganglia output nuclei, defective neural inhibition at the spinal, brainstem, cortical level and sensorimotor misprocessing. More recently, increased neural plasticity has been found in dystonia patients in response to transcranial magnetic stimulation (TMS) protocols which induce motor cortex plasticity. Excessive plasticity might contribute to dystonia by promoting or reinforcing abnormal patterns of connectivity. The most significant advance in the treatment of generalised dystonia has been the development of globus pallidus internus (GPi) deep brain stimulation (DBS). Interestingly its beneficial effects are progressive over weeks to months rather than immediate. A plasticity effect has been implicated but physiological evidence has been lacking. Furthermore it is unknown what impact GPi DBS has on the underlying pathophysiology such as defective inhibition or excessive plasticity. The aim of the present work was to examine the impact of GPi DBS on underlying pathophysiological features such as disinhibition and abnormal motor cortical plasticity. In this thesis, studies in a consecutive series of dystonia patients, mainly those with primary generalised dystonia, who underwent bilateral GPi DBS, are presented. Patients were studied in a prospective, longitudinal manner with both clinical assessment of dystonia using a validated rating scale and electrophysiological studies including blink reflex excitability and forearm H-reflex reciprocal inhibition. In addition, once stable improvement had been achieved, the impact of GPi DBS on motor cortex plasticity was studied using TMS paired associative stimulation (PAS). The clinical study of these patients confirmed the therapeutic efficacy of GPi DBS and provided direct evidence of the superiority of the posteroventral globus pallidus as the optimal target. The longitudinal studies of blink and H-reflex, showed progressive normalisation of brainstem and spinal excitability, which correlated with the time-course of clinical improvement. These data provide the first evidence of reversal of underlying dystonia pathophysiology by GPi DBS and are compatible with progressive long-term neural reorganisation (plasticity) playing a role in the mechanism of action of GPi DBS. Furthermore, the result of TMS PAS experiments demonstrated that GPi DBS reduces the short-term plasticity of the motor cortex, the magnitude of this effect also correlated with therapeutic effect. This result is compatible with the concept that excessive plasticity promotes dystonia and reversal of these abnormalities may be another mechanism by which GPi DBS acts. In conclusion, work presented in this thesis provides the first electrophysiological correlates of clinical improvement in dystonia after GPi DBS, which collectively supports the notion that both long and short-term plasticity within the central nervous system are involved in the mechanism of GPi DBS action.
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Yancey, Madison E. "Computational Simulation and Analysis of Neuroplasticity." Wright State University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=wright1622582138544632.

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Thompson, Karen Louise Elliott. "Ear manipulations help model neuroplasticity limitations." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/4969.

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Sensory organs, such as the inner ear, send information about the outside world to the central nervous system (CNS) through afferent neurons and in turn, the CNS sends information back to certain sensory organs through efferent neurons to modulate the incoming signal. Though how these afferent and efferent neurons navigated with their processes to the hindbrain or hair cells, respectively, is not clear. By transplanting ears to other locations, or adding ears, we can effectively create a novel ear to ask how the CNS adapts to a new sensory system, complete with efferent innervation of hair cells and afferent innervation into the CNS. In addition, by removal of the existing ear, we can ask what influence an established sensory system has on CNS development. Transplantation of Xenopus laevis ears caudally to the trunk to replace a somite or to the orbit to replace the eye resulted in the innervation of hair cells of the transplanted ear by spinal motor neurons or by oculomotor and trochlear motor neurons, respectively. The ability to be innervated by any motor neuron is a unique property associated with inner ear hair cells as other tissues normally receiving motor innervation were not innervated by all motor neurons when transplanted. Projections of inner ear afferents into the CNS when the ear was transplanted to the orbit were inconsistent, but occasionally projected into the vestibular nucleus along the trigeminal nerve, suggesting that there may be molecular guidance of inner ear afferents if they projected by chance near the vicinity of the vestibular nucleus. The eye, which is developmentally related to the ear, uses both molecular targeting to the CNS and once there, projections from the two eyes are refined through activity-based mechanisms. Transplantation of an additional ear rostral to the native ear in Xenopus laevis in either the native orientation or rotated 90 degrees with respect to the native ear showed that axons from the two ears project to the vestibular nucleus, likely using molecular cues. Furthermore, axons from the natively-oriented transplanted ear overlap with axons from the native ear, and in contrast, axons from the rotated transplanted ear segregate from those of the native ear. The latter is likely due to differential activity between the two ears and suggests that the ear uses similar mechanisms as the eye for axon guidance. The effect of ear removal has been well studied on populations of hindbrain neurons, but less at the single-cell level. Removal of an ear demonstrated the dependence of the ear for the development and/or survival of a target cell of the ear, the Mauthner cell, but only for a critical time in development. Furthermore, ear ablation resulted in the reduction of the number of dendritic branches in surviving Mauthner cells and an increase in dendritic branching when an extra ear was transplanted rostral to the native ear, suggesting a relationship between sensory afferent input and dendritic development of a target neuron. Together these results show that the nervous system can adapt to a novel sensory system, but with limitations, especially in sensory afferent guidance. In addition, perturbations of an established system have consequences on the development of target neurons dedicated for that system.
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Jacques, Angela. "Investigating the neuroplasticity of emotional memories." Thesis, Queensland University of Technology, 2019. https://eprints.qut.edu.au/132644/1/Angela_Jacques_Thesis.pdf.

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This study in behavioural neuroscience assists in identifying the cellular and molecular mechanisms underlying cognitive brain functions in relation to processing emotions. The thesis identifies how neuroplastic change impacts neuropsychiatric disease states and examines a behavioural model of fear memory recall to detail the neuronal circuits, neurotransmitters and some of the cellular mechanisms involved. Investigation of neural substrates and neuroplastic change may facilitate the development of increasingly effective pharmacotherapeutics and contribute to the creation of abiding treatments for anxiety related disorders.
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Books on the topic "Neuroplasticity"

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Costa e Silva, J. A., J. P. Macher, and J. P. Olié, eds. Neuroplasticity. Tarporley: Springer Healthcare Ltd., 2009. http://dx.doi.org/10.1007/978-1-908517-18-0.

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Raskin, Sarah A. Neuroplasticity and rehabilitation. New York: Guilford Press, 2011.

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A, Shaw Christopher, and McEachern Jill C, eds. Toward a theory of neuroplasticity. Philadelphia: Psychology Press, 2001.

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J, Handa Robert, ed. Neuroplasticity, development, and steroid hormone action. Boca Raton, FL: CRC Press, 2001.

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Pearce, Alan J. Neuroplasticity following skill and strength training. Hauppauge, N.Y: Nova Science, 2010.

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Carmesin, Hans-Otto. Theorie neuronaler Adaption. Berlin: Köster, 1994.

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Fox, Gerard B. Behavioural, functional and pharmacological modulation of rodent neural cell adhesion molecule mediated neuroplasticity. Dublin: University College Dublin, 1995.

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International Symposium on "Plasticity of Synapse and Neural Networks in the Brain" (4th 1994 Okazaki-shi, Japan). Plasticity of synapse and neural networks in the brain: Fourth International Symposium on "Plasticity of Synapse and Neural Networks in the Brain" ... National Institute for Physiological Sciences, Okazaki, Japan, January 26-28, 1994. Edited by Ebashi Setsurō 1922-, Ohmori Harunori, Yamagishi S, Biomedical Research Foundation (Japan), and Seirigaku Kenkyūjo (Japan). Tokyo: Biomedical Research Foundation, 1994.

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L, McGaugh James, Weinberger Norman M, Lynch Gary, and University of California, Irvine. Center for the Neurobiology of Learning and Memory., eds. Brain and memory: Modulation and mediation of neuroplasticity. New York: Oxford University Press, 1995.

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Uzbay, Tayfun. A new approach to etiopathogenezis of depression: Neuroplasticity. Hauppauge, N.Y: Nova Science Publisher, 2011.

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Book chapters on the topic "Neuroplasticity"

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Fuchs, Eberhard. "Neuroplasticity — A New Approach to the Pathophysiology of Depression." In Neuroplasticity, 1–12. Tarporley: Springer Healthcare Ltd., 2011. http://dx.doi.org/10.1007/978-1-908517-18-0_1.

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Reznikov, Leah R., Jim R. Fadel, and Lawrence P. Reagan. "Glutamate-Mediated Neuroplasticity Deficits in Mood Disorders." In Neuroplasticity, 13–26. Tarporley: Springer Healthcare Ltd., 2011. http://dx.doi.org/10.1007/978-1-908517-18-0_2.

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Svenningsson, Per, and Bruce S. McEwen. "Regulation of Cellular Plasticity in Mood Disorders: The Role of the AMPA Receptor." In Neuroplasticity, 27–39. Tarporley: Springer Healthcare Ltd., 2011. http://dx.doi.org/10.1007/978-1-908517-18-0_3.

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Jay, Thérèse M. "Cellular Plasticity and the Pathophysiology of Depression." In Neuroplasticity, 41–55. Tarporley: Springer Healthcare Ltd., 2011. http://dx.doi.org/10.1007/978-1-908517-18-0_4.

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Gorwood, Philip. "Clinical Consequences of the Role of Glutamate and Neuroplasticity in Depressive Disorder." In Neuroplasticity, 57–68. Tarporley: Springer Healthcare Ltd., 2011. http://dx.doi.org/10.1007/978-1-908517-18-0_5.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Neuroplasticity." In Encyclopedia of Psychopharmacology, 856. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_442.

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Wenger, Elisabeth, and Simone Kühn. "Neuroplasticity." In Cognitive Training, 69–83. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39292-5_6.

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Boutzoukas, Emanuel M., and Adam J. Woods. "Neuroplasticity." In Encyclopedia of Gerontology and Population Aging, 1–5. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69892-2_678-1.

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Mishra, Ramesh Kumar. "Neuroplasticity." In Cognitive Science, 100–129. London: Routledge India, 2022. http://dx.doi.org/10.4324/9781003316053-5.

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Joshua, Abraham M. "Neuroplasticity." In Physiotherapy for Adult Neurological Conditions, 1–30. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-0209-3_1.

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Conference papers on the topic "Neuroplasticity"

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Alvarez, Tara L., Yelda Alkan, Eun Kim, Rajbir Jaswal, Diana Ludlam, Phillipe Moinot, Bharat B. Biswal, and Vincent R. Vicci. "Neuroplasticity in vision dysfunction." In 2009 4th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2009. http://dx.doi.org/10.1109/ner.2009.5109280.

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Ochs, Karlheinz, Dennis Michaelis, Sebastian Jenderny, and Hermann Kohlstedt. "Mimicking Neuroplasticity by Memristive Circuits." In 2020 IEEE 63rd International Midwest Symposium on Circuits and Systems (MWSCAS). IEEE, 2020. http://dx.doi.org/10.1109/mwscas48704.2020.9184515.

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Parija, Rohan, and Nongmeikapam Thoiba Singh. "Neuroplasticity Changes to Configure Human Talent." In 2023 International Conference on Circuit Power and Computing Technologies (ICCPCT). IEEE, 2023. http://dx.doi.org/10.1109/iccpct58313.2023.10245239.

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Dragunas, Guilherme, Natalia De Souza Xavier Costa, Reinoud Gosens, Carolina Demarchi Munhoz, and Thais Mauad. "Neuroimmune interactions and neuroplasticity in fatal asthma." In ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa2984.

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Dragunas, Guilherme, Manon Woest, Susan Nijboer, Sophie Bos, Corneel Vermeulen, Ben Ditz, Judith Vonk, et al. "BDNF-TrkB signaling mediates cholinergic neuroplasticity in asthma." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa4957.

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Novais, Aurea Maria Lago, and Renan Carvalho Castello Branco. "Mechanisms of Neuroplasticity After Pediatric Stroke: A Review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.241.

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Introduction: Stroke in childhood constitute a rare event and its incidence is increasing due to advances in neuroimaging.This study clarifies anatomic and molecular mechanisms involved in neuroplasticity after children stroke, demonstrating its specificities in motor,somatosensory and language habilities. Methods: We used database, from 2000 to march 2021,of SpringerLink,NEJM,PubMed, AHA (Stroke),Scielo,VHL and JAMA.The research was based in the keywords “neuplasticity”, “stroke” and “children”; 57 were selected including original articles, case reports and reviews, considering abstract according to the objective of the present study and methodologies that satisfy criterias of cientific valuation, considering p <0,005 as statistical significance. Results: Reduction of ipsilesional cortex and better prognosis between the ages of 1 and 6 years were observed. About motor function, it was found persistence of some perilesionais circuits, contralateral reorganization with increasing activation of suplementary motor area, unbalance of intrahemisferics inhibitory mechanisms, increase of excitability and changes in the concentration of N-acetyl-aspartate, choline, myo-inositol and creatine. Somatosensory skills presented limited plasticity. Contralesional alterations in arched fasciculi and temporoparietal area, circuit remodelation and compromissing of complex cognitive functions were observed for language habilites. Conclusion: Better outcomes in the ages of 1 to 6 years demonstrate the duality between early vulnerability and early plasticity. The plasticity of motor system demonstrates therapeutic targets and potencial rehabilitation markers; otherwise, the limited potencial of somatossensorial habilities indicates its premature determination. Language skills presented limited prognosis.
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Danyar, Mikkel Bjerre, Hjalte Föerregård Clark, Nickolaj Ajay Atchuthan, Lasse Krøgh Daugbjerg, Amalie Koch Andersen, Taha Al Muhammadee Janjua, and Winnie Jensen. "Spatio-Temporal Analysis of LTP-like Neuroplasticity in Pigs." In 2023 11th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2023. http://dx.doi.org/10.1109/ner52421.2023.10123814.

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Rahimi, Masoumeh, Lauren E. Margulieux, James Prather, Gozde Cetin Uzun, and Bailey Kimmel. "Benefits of Failure on Neuroplasticity and Tools for Persistence." In ICER 2023: ACM Conference on International Computing Education Research. New York, NY, USA: ACM, 2023. http://dx.doi.org/10.1145/3568812.3603470.

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Jääskö-Santala, Kati. "Finnish Teachers’ Mindsets and Conceptions of Neuroplasticity (Poster 40)." In 2024 AERA Annual Meeting. Washington DC: AERA, 2024. http://dx.doi.org/10.3102/2095472.

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Jääskö-Santala, Kati. "Finnish Teachers’ Mindsets and Conceptions of Neuroplasticity (Poster 40)." In AERA 2024. USA: AERA, 2024. http://dx.doi.org/10.3102/ip.24.2095472.

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Reports on the topic "Neuroplasticity"

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Li, He, Maria Braga, Chris Hough, Sean Manion, Xiaolong Jiang, Aiquin Chen, Eleanore H. Gamble, Preetha Abraham, and V> Anderjaska. Neuroplasticity and Calcium Signaling in Stressed Rat Amygdala. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada435451.

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Shah, Sikandar. Ketamine: Benefits and Risks for Depression, PTSD & Neuroplasticity | Huberman Lab Podcast. ResearchHub Technologies, Inc., August 2023. http://dx.doi.org/10.55277/researchhub.7cfhtrjx.

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You might also be interested in the extended bibliographies on the topic 'Neuroplasticity' for particular source types:
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