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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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Hakim, Marziah. "Neurogenesis and neuroplasticity following olfactory fear conditioning." Thesis, Queensland University of Technology, 2019. https://eprints.qut.edu.au/157474/1/Marziah_Hakim_Thesis.pdf.
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This dissertation focused on determining the neurocircuitry of olfactory fear conditioning in order to further understand the microanatomy of post-traumatic stress disorder and contribute towards the refinement of therapeutic innovations. The study determined that different subnuclei of the amygdala were involved in olfactory fear memory and that recollection of such memories enhanced neuroplasticity and increased the number of new born neurons and astrocytes in the brain regions associated with olfaction and memory processing. This study concluded that following olfactory fear conditioning, newborn neurons may undergo long term potentiation, which may support their survival up to 14 days after birth.
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Yeung, Luk Chong. "A mechanistic model of calcium-dependent synaptic plasticity /." View online version; access limited to Brown University users, 2005. http://wwwlib.umi.com/dissertations/fullcit/3174704.
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Yuan, Wujie. "Adaptive networks and synaptic plasticity in neural systems : interplay between structure and dynamics." HKBU Institutional Repository, 2012. https://repository.hkbu.edu.hk/etd_ra/1398.
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Guegan, Thomas 1983. "Common neuroplasticity mechanisms underlying drugs and food reward." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/125444.
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Drug addiction and some eating disorders present striking similarities in their behavioural symptoms. It has been postulated that excessive consumption of drugs of abuse and palatable food could lead to the development of similar neuronal alterations in the brainreward circuit that may account for the resemblance of these pathologies. In the present thesis, we demonstrate that repeated operant training with palatable food promotes behavioural alterations and structural plasticity changes in the esocorticolimbic circuit that are reminiscent to those observed with drugs of abuse. Furthermore, we identify the cannabinoid receptor 1 as a common neurobiological substrate underlying these alterations. Finally, we uncover several synaptic proteins commonly implicated in the retrieval of drug and palatable food rewarding memories that may represent part of the common neurobiological basis underlying drug and palatable food craving.La adicción a las drogas de abuso y determinados trastornos alimentarios comparten varios síntomas comportamentales. Algunos estudios han sugerido que el consumo excesivo de drogas y de comida palatable podrían producir alteraciones neuronales similares en el circuito cerebral de recompensa. En esta tesis, hemos demostrado que un aprendizaje operante prolongado con comida palatable provoca la aparición de alteraciones comportamentales y cambios de plasticidad estructurales en el circuito mesocorticolimbico que son reminiscentes de los observados con las drogas de abuso. Así mismo, hemos identificamos al receptor cannabinoide 1 como un sustrato neurobiológico común a estas alteraciones. Finalmente, hemos caracterizado varias proteínas sinápticas implicadas en la reactivación de la memoria asociada a los efectos placenteros de las drogas y la comida palatable. Nuestras observaciones contribuyen a definir las bases neuronales subyacentes a la necesidad de consumir drogas y comida palatable.
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Shetty, Kunal. "Motor learning induced neuroplasticity in minimally invasive surgery." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/56079.
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Technical skills in surgery have become more complex and challenging to acquire since the introduction of technological aids, particularly in the arena of Minimally Invasive Surgery. Additional challenges posed by reforms to surgical careers and increased public scrutiny, have propelled identification of methods to assess and acquire MIS technical skills. Although validated objective assessments have been developed to assess motor skills requisite for MIS, they poorly understand the development of expertise. Motor skills learning, is indirectly observable, an internal process leading to relative permanent changes in the central nervous system. Advances in functional neuroimaging permit direct interrogation of evolving patterns of brain function associated with motor learning due to the property of neuroplasticity and has been used on surgeons to identify the neural correlates for technical skills acquisition and the impact of new technology. However significant gaps exist in understanding neuroplasticity underlying learning complex bimanual MIS skills. In this thesis the available evidence on applying functional neuroimaging towards assessment and enhancing operative performance in the field of surgery has been synthesized. The purpose of this thesis was to evaluate frontal lobe neuroplasticity associated with learning a complex bimanual MIS skill using functional near-infrared spectroscopy an indirect neuroimaging technique. Laparoscopic suturing and knot-tying a technically challenging bimanual skill is selected to demonstrate learning related reorganisation of cortical behaviour within the frontal lobe by shifts in activation from the prefrontal cortex (PFC) subserving attention to primary and secondary motor centres (premotor cortex, supplementary motor area and primary motor cortex) in which motor sequences are encoded and executed. In the cross-sectional study, participants of varying expertise demonstrate frontal lobe neuroplasticity commensurate with motor learning. The longitudinal study involves tracking evolution in cortical behaviour of novices in response to receipt of eight hours distributed training over a fortnight. Despite novices achieving expert like performance and stabilisation on the technical task, this study demonstrates that novices displayed persistent PFC activity. This study establishes for complex bimanual tasks, that improvements in technical performance do not accompany a reduced reliance in attention to support performance. Finally, least-squares support vector machine is used to classify expertise based on frontal lobe functional connectivity. Findings of this thesis demonstrate the value of interrogating cortical behaviour towards assessing MIS skills development and credentialing.
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Oliver, Chicora. "CHEMOKINE MODULATION OF MDPV-INDUCED BEHAVIOR AND NEUROPLASTICITY." Diss., Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/596047.
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PsychologyPh.D.
Psychostimulant abuse is a major public health concern yet no FDA-approved medications exist. Synthetic cathinones (“bath salts”) are a class of psychostimulants that have emerged relatively recently worldwide. One synthetic cathinone, MDPV (3,4-methylenedioxypyrovalerone) is mechanistically similar to cocaine but is over ten times more potent, possesses high abuse potential, and is relatively understudied. Recent studies have revealed involvement of inflammatory proteins called chemokines in the rewarding effects of MDPV and the mechanistically similar drug, cocaine. We and others have shown that the chemokine-receptor ligand pair CXCL12-CXCR4 is recruited in the rewarding effects of cocaine and MDPV. Humans and animal models of cocaine addiction have dysregulated CXCL12 and the commercially-available CXCR4 antagonist, AMD3100, can reverse cocaine use and relapse in preclinical models of addiction. Specifically, AMD3100 reduces self-administration and reinstatement to cocaine-seeking with concomitant alterations in CXCL12 gene expression in the midbrain. Here, I employ several complementary methods to demonstrate that AMD3100 also reverses MDPV-elicited behaviors. I demonstrate that (i) AMD3100 reverses MDPV-induced hyperlocomotion, conditioned place preference (preclinical model of drug reward), self-administration and reinstatement to MDPV-seeking behavior; (ii) AMD3100 can rescue MDPV-induced deficits in measures of anxiety and recognition memory shortly after a binge; and (iii) repeated MDPV exposure upregulates CXCL12 gene expression in the nucleus accumbens with concomitant downregulation of dendrite morphometrics and a related synapse scaffolding protein gene expression. These findings implicate CXCR4-CXCL12 signaling in the modulation of MDPV-elicited behaviors, suggesting that AMD3100 is a viable therapeutic option for the effects of this synthetic cathinone.
Temple University--Theses
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Catuara, Solarz Silvina 1986. "Neuroplasticity-targeted therapy for Down syndrome: a translational approach." Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/523544.
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This Thesis aims at addressing the therapeutic potential of a neuroplasticity-targeted treatment for intellectual disability (ID) in Down syndrome (DS). The therapy consisted of the administration of the green tea catechin Epigallocatechin-3-gallate (EGCG), which is a natural modulator of Hsa21 candidate genes Dyrk1A and APP, in combination with cognitive stimulation. The assessment of the therapeutic efficacy of this intervention was performed using a translational approach, including preclinical studies with a mouse model of DS and clinical trials with humans with DS.
In this work we show for the first time that this combined therapy significantly ameliorates cognitive deficits in mice and young adults with DS, by modifying brain neuronal networks structure and function.Esta Tesis tiene como objetivo examinar el potencial terapéutico de una intervención orientada a mejorar la neuroplasticidad cerebral, propuesta para mitigar la discapacidad intelectual (DI) en el síndrome de Down (SD). La terapia consistió en la administración de la catequina del té verde, Epigalocatequina-3-galato (EGCG), que es un modulador natural de dos genes candidatos que se encuentran en Hsa21, Dyrk1A y APP, en combinación con estimulación cognitiva. La evaluación de la eficacia terapéutica de esta intervención se realizó utilizando un enfoque de la translacional, incluyendo estudios preclínicos con un modelo de ratón de SD y ensayos clínicos con adultos jóvenes con SD. Este trabajo demuestra por primera vez que esta terapia combinada atenúa significativamente los déficits cognitivos en ratones y adultos jóvenes con SD, mediante la modificación de la estructura y función de redes neuronales en el cerebro.
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Hamrahi, Hormoz. "Neuroplasticity in the cochlear nucleus of the developing chinchilla." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ34087.pdf.
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Klinger, Mary Beth. "Neuroplasticity of Micturition Reflex Pathways with Cyclophosphamide-Induced Cystitis." ScholarWorks @ UVM, 2008. http://library.uvm.edu/dspace/bitstream/123456789/173/1/marybethklingerfinal.pdf.
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Wong, Scott Thaddeus. "Role of the calcium-stimulated adenylyl cyclases in neuroplasticity /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/6300.
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林綺鈴 and Yee-ling Lam. "Proheparanase action at excitatory synapses : implication on synaptic plasticity." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/193096.
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Synaptic plasticity is the activity-dependent modification of the strength of synaptic transmission. It is important for learning and memory. One of the mechanisms mediating synaptic plasticity at glutamatergic synapses is regulation of the postsynaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptor (AMPAR), which governs excitatory synaptic transmission. Perineuronal heparan sulfates (HS) have been implicated in controlling the open-state of AMPARs. Earlier findings in our laboratory showed heparanase expression and secretion of proheparanase by hippocampal neurons. Recombinant proheparanase triggered neuronal co-internalization of HS-proteoglycans and AMPAR subunits; this led to decreases in basal synaptic strength and long term potention of synaptic transmission at Schaffer collateral synapses of the hippocampus. The findings suggested proheparanase acting as a negative regulator of synaptic plasticity but the underlying mechanism remained unclear. We hypothesized that neuronal secretion of proheparanase is localized toperi-synaptic regions such that proheparanase mediates clustering of peri-synaptic HS-proteoglycans and AMPARs for internalization of the protein cluster.
To address this, protein kinase C-mediated secretion of proheparanase was enhanced by phorbol ester treatment of hippocampal slices. Synaptosome preparations from the treated slices indicated enrichment in proheparanase, suggesting that proheparanase was directed to synaptic terminals for localized secretion. With use of the hippocampal synaptosomes, pull-down experiments targeting syndecan-3and heparanase found AMPAR subunits, both GluR1 and GluR2/3, indicating that they formed clusters in the peri-synaptic area. Heparitinase pre-treated hippocampal neurons in culture led to lower levels of internalized AMPAR subunits, both GluR1 and GluR2/3,upon recombinant proheparanase treatment. This suggested that HS moieties were critical for proheparanase-mediated AMPAR internalization. Recombinant proheparanase treatment of the neuronal cultures also led to decreases in glutamate-induced calcium influx, in terms of both the number of responsive cells and the change in intracellular calcium level, consistent with proheparanase-mediated neuronal internalization of AMPARs. Taken together, these results support our hypothesis and highlight dependence on the HS moiety for proheparanase-mediated neuronal internalization of AMPARs.
We further investigated if proheparanase action at synapses can be found in other brain regions. The finding of neuronal heparanase expression in vestibular nucleus (VN) microexplant culture led us to study the role of proheparanase in synaptic plasticity in the VN. PKC activation enhanced heparanase expression in VN microexplant cultures. Recombinant proheparanase also triggered the uptake of HS and led to decreases in glutamate-induced calcium influxin VN microexplant cultures. These results support that proheparanase plays a role in synaptic plasticity in the VN but the effect and mechanism of action of proheparanase in VN neurons remain to be elucidated.
This study demonstrated that neuronal secretion of proheparanase at synaptic terminals regulates AMPAR internalization, resets peri-synaptic HS levels and lowers calcium dependent signaling in responsive cells. This work has revealed a novel role of neuronal proheparanase in synaptic plasticity.published_or_final_version
Biochemistry
Master
Master of Philosophy
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Pons, Espinal Meritxell 1986. "Role of DYRK1A in hippocampal neuroplasticity : implications for Down syndrome." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/124485.
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Synaptic connections in the brain respond throughout their lives to the activity of incoming neurons, adjusting their biological properties to increment activity-dependent changes. Hippocampal neuronal plasticity disruptions have been suggested as mechanisms underlying cognitive impairments in Down syndrome (DS). However, it remains unknown whether specific candidate genes are implicated in these phenotypes in the multifactorial context of trisomy 21. DYRK1A is a serine/threonine kinase, which overexpression is sufficient to recapitulate hippocampal learning and memory deficits characteristic of DS individuals and trisomic mouse models. In this Thesis we have studied the effects of DYRK1A overexpression on activity-dependent plasticity in the hippocampus. We found that transgenic mice overexpressing Dyrk1A (TgDyrk1A) present hippocampal morphological alterations in CA1 and CA3 that may constrain network connectivity, and therefore are relevant to the structure-function relationship. We also found reduced LTP that may derive from the changes in connectivity and in dendritic occupancy. Dendritic excitability and neuronal morphology are determinants of synaptic efficacy and thus may contribute to the hippocampal learning and memory deficits detected. In addition, we demonstrated important defects in adult neurogenesis in the dentate gyrus including reduced cell proliferation rate, altered cell cycle progression and reduced cell cycle exit leading to premature migration, altered differentiation and reduced survival of newly born cells. Moreover, less proportion of newborn hippocampal TgDyrk1A neurons are activated upon learning, suggesting reduced integration in learning circuits. Some of these alterations were rescued by normalizing DYRK1A kinase using a DYRK1A inhibitor, epigallocatechin-3-gallate. Interestingly, environmental stimulation also normalized DYRK1A kinase overdosage in the hippocampus, and rescued hippocampal morphology, synaptic plasticity and adult neurogenesis alterations in TgDyrk1A mice. We conclude that Dyrk1A is a good candidate gene to explain neuronal plasticity deficits in DS and that targeting DYRK1A kinase activity excess either pharmacologically or using environmental stimulation in the adult could correct these defects in DS.Les connexions sinàptiques tenen la capacitat de respondre a l’activitat de neurones ajustant les seves propietats biològiques per incrementar els canvis activitat-depenents. Alteracions en la plasticitat neuronal de l’hipocamp s'han suggerit com a mecanismes subjacents als deterioraments cognitius característics en la síndrome de Down (SD). No obstant, es desconeix quins gens específics estan implicats en aquests fenotips en el context de la trisomia del cromosoma 21. DYRK1A és una serina / treonina quinasa, que quan es troba sobreexpressada recapitula el dèficit d'aprenentatge i de memòria depenent de l'hipocamp característic de la SD. En aquesta tesi, s’han estudiat els efectes de la sobreexpressió de DYRK1A en la plasticitat activitat-dependent de l’hipocamp. Hem descobert que ratolins transgènics amb sobreexpressió de Dyrk1A (TgDyrk1A) presenten alteracions morfològiques en les regions CA1 i CA3 de l'hipocamp, una limitació estructural en les connexions neuronals que és rellevant per entendre la relació entre estructura i funció. A més, hem trobat una reducció en la LTP possiblement deguda als canvis en la connectivitat i ocupació dendrítica. L’excitabilitat de les dendrites i la morfologia neuronal són factors determinants de l'eficàcia sinàptica i per tant poden contribuir als dèficits d'aprenentatge i la memòria de l'hipocamp detectats. Hem demostrat defectes importants en la neurogènesi adulta en el gir dentat incloent una reduïda taxa de proliferació cel·lular, alteracions en el cicle cel·lular i reducció de cèl·lules que surten del cicle cel·lular que condueix a una migració precoç de les noves cèl·lules generades i una reducció de la supervivència. D'altra banda, en ratolins TgDyrk1A hi ha menys proporció de neurones generades de novo que s'activen amb l'aprenentatge, indicant una menor integració d’aquestes en els circuits implicats en l'aprenentatge. Algunes d'aquestes alteracions han estat rescatades per la normalització de DYRK1A quinasa utilitzant un inhibidor de DYRK1A, epigallocatechin-3-gallate. L'estimulació del medi ambient també normalitza la sobreexpressió de DYRK1A quinasa en l'hipocamp, i rescata la morfologia, la plasticitat sinàptica i les alteracions en la neurogènesi adulta en ratolins TgDyrk1A. Arribem a la conclusió que Dyrk1A és un bon gen candidat per explicar els dèficits de plasticitat neuronal en la SD i que tractant l’excés d'activitat de la quinasa DYRK1A farmacològicament o mitjançant l'estimulació ambiental en l'adult podria corregir aquests defectes en la SD.
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Adams, Louise. "Promotion of neuroplasticity by modifying perineuronal nets using polysialic acid." Thesis, Queen Mary, University of London, 2017. http://qmro.qmul.ac.uk/xmlui/handle/123456789/24547.
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Polysialic acid (PSA) is a linear homopolymer formed of chains of 2,8-linked sialic acid. Found predominantly attached to the neural cell adhesion molecule, PSA acts to reduce cell-cell adhesion during development. It is also found in some areas of the adult central nervous system (CNS) associated with persistent neuroplasticity. Preliminary data from our laboratory indicated an inverse relationship between PSA expression and the formation of perineuronal nets (PNNs), specialised extracellular matrix structures with a role in limiting plasticity in the adult CNS. The primary aims of this thesis were to investigate this relationship in more detail, using in vitro models of PNN formation and in vivo. Also, to evaluate whether lentiviral vector-mediated PSA expression can enhance locomotor recovery and neuroplasticity in a rodent model of spinal cord injury. PNNs were heterogeneously distributed throughout the grey matter of the rat cervical spinal cord, and increased in numbers down the dorsoventral axis. Induced expression of PSA in the spinal cord of either naïve or injured rats did not alter the number or density of PNNs. Similarly, enzymatic removal of PSA from the surface of cultured embryonic neurons did not affect the formation of the PNNs. In a rodent model of cervical spinal cord injury, induced PSA expression resulted in an improvement in hindlimb, but not forelimb, locomotor function compared to animals injected with control virus. Interestingly, this was not associated with an increased density of serotonin or synaptophysin-labelled boutons in the areas of induced PSA expression. Taken together, the data presented in this thesis suggests that while induced PSA expression may contribute to improved locomotor function in a model of cervical spinal cord injury, this is not due to a reduction in the density or number of PNNs in the spinal cord.
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Alia, Claudia. "Studying and modulating post-stroke neuroplasticity to improve motor recovery." Doctoral thesis, Scuola Normale Superiore, 2016. http://hdl.handle.net/11384/86002.
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Limited restoration of motor function occurs spontaneously during a plastic time window after stroke. A deeper understanding of post-stroke plasticity is critical to devise more effective pharmacological and rehabilitative treatments.
Here, I have characterized the spontaneous evolution after a photothrombotic lesion in mice, both in terms of motor deficit and plasticity in the perilesional cortex. In generalized motor tasks such as the Gridwalk and Schallert Cylinder test, motor deficits were stable for at least 30 days after photothrombotic stroke in the Caudal Forelimb Area (CFA). The skilled reaching test, performed once a week, showed a trend for spontaneous improvement over time in the number of correct graspings. However, kinematic analysis, evaluated by means of an innovative semi-automated tool, revealed a persistent alterations in grasping movements, pointing to the development of compensatory strategies.
The perilesional cortex has been proposed as the area mediating functional recovery. I found a reorganization of the motor maps in sensorimotor cortex around to the lesion. Particularly, I observed a significant shrinkage of the forelimb area, in favour of hindlimb representation using Intracortical Microstimulation (ICMS). Moreover, neuroanatomical markers, previously characterized in the literature as “neuroplasticity brakes” (i.e. Perineuronal nets, Parvalbumin- and Somatostatin-positive cells) spontaneously decrease after stroke, suggesting an enhancement of the potential for plastic rearrangements. Altogether these results, suggest a spontaneous attempt to reopen a critical period characterized by sprouting and plasticity phenomena, that needs to be amplified and properly guided for maximizing recovery.
The GABAergic system is one of the key modulators of plasticity in the brain, and its role has been amply studied in relation to opening and closure of the “critical period” in sensory cortices during development. To test whether reductions in GABAergic signalling were causally involved in motor improvements, we treated animals during an early post-stroke period with a benzodiazepine inverse agonist, which impairs GABAA receptor function. We found that hampering GABAA signalling led to significant restoration of function in general motor tests such as the gridwalk and the pellet reaching tasks, with no significant impact on the kinematics of reaching movements. Improvements were persistent as they remained detectable about three weeks after treatment.
Using electrophysiological recordings I found an electrical imbalance between the two hemispheres. In particular, contralesional motor cortex was found to exert an enhanced transcallosal inhibition over the spared, perilesional tissue. Silencing the healthy hemisphere using cortical infusion of Botulinum Neurotoxin E, partially improved motor recovery in the gridwalk test.
We then established a rehabilitation protocol that combined intensive and highly repeatable exercise of the mouse forelimb with a robotic platform with reversible inactivation of the healthy, contralesional motor cortex. We found that such treatment promoted recovery in both Gridwalk and Schallert Cylinder tests and in end point measures during Skilled reaching test. Remarkably, the combined therapy also restores pre-lesion movement patterns during reaching movement, as evaluated by kinematic analysis. Furthermore, such rehabilitated animals showed a more plastic perilesional cortex, with an additional significant decrease in plasticity brakes.
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Ma, Chun-wai. "Study of perineuronal nets in plasticity of central circuitry." Click to view the E-thesis via HKUTO, 2010. http://sunzi.lib.hku.hk/hkuto/record/B43914524.
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Xu, Bin. "Axonal growth, neuronal damage and epileptogenesis /." *McMaster only, 2002.
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Ma, Chun-wai, and 馬俊偉. "Study of perineuronal nets in plasticity of central circuitry." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B43914524.
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Sánchez-Duran, José Antonio. "Neural plasticity in premotor pathways of the Aplysia feeding system : short-term synaptic modulation of motor programs, synaptic interactions, regeneration of cerebral-buccal connections, and recovery of buccal motor programs /." free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3013019.
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Wainwright, Steven R. "Androgens and neuroplasticity : contributions to the pathogenesis and treatment of depression." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/55848.
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Depression is a devastating neuropsychiatric disease that has profound effects on neural structure and function, however the pathogenesis and modes of effective treatment remain poorly understood. Stress is the primary preceding factor in depression, leading to profound deficits in neurophysiology, particularly in the hippocampus. Depressed patients show reduced hippocampal neuroplasticity, while antidepressant treatment enhances both neurogenesis and the expression of proteins that mediate plasticity such as the polysialylated form of the neural cell adhesion molecule (PSA-NCAM). Interestingly, men are half as likely as women to develop depression, where androgens appear to confer resiliency in males, as hypogonadal men are more likely to develop depression and supplementation of testosterone shows antidepressant efficacy. Little is known about the neurological underpinnings of this profound sex difference, however androgens influence the stress response and enhance hippocampal neurogenesis. The experiments in this thesis aimed to examine the role of androgens in the pathogenesis and treatment of depression using an animal model, with a specific eye toward the impact on hippocampal neurogenesis and neuroplasticity, and whether neuroplasticity mediated through PSA-NCAM is essential to antidepressant efficacy. In Chapter 2, surgically-induced hypogonadism potentiates the expression of depressive-like endophenotypes in male rodents within a chronic unpredictable stress (CUS) model of depression. Hypogonadal males showed potentiated behavioural, endocrine, and neurophysiological depressive-like phenotypes, including reductions in hippocampal neurogenesis and the expression of PSA-NCAM, compared to intact males. In Chapter 3, the hypogonadism-induced susceptibility to depressive-like phenotypes following CUS is largely inhibited by supplementation with testosterone. Testosterone treatment ameliorated physiological and endocrine phenotypes while showing independent antidepressant-like effects and facilitating the efficacy of an antidepressant drug in some measures. In Chapter 4, the enzymatic cleavage of the polysialic acid moiety from NCAM completely inhibits the behavioural efficacy of antidepressant treatment, while also serving to attenuate the survival of newly generated hippocampal neurons. Collectively, this body of research demonstrates the protective effects of androgens against the development of depression in males, coinciding with enhanced hippocampal neuroplasticity, and delineates an essential role for neuroplasticity mediated through PSA-NCAM in antidepressant action.Medicine, Faculty of
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Rossi, Sonja [Verfasser], Heather [Gutachter] Bortfeld, and Erich [Gutachter] Schröger. "Neuroplasticity of word learning / Sonja Rossi ; Gutachter: Heather Bortfeld, Erich Schröger." Berlin : Humboldt-Universität zu Berlin, 2018. http://d-nb.info/1185579176/34.
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Wansbrough, Kym. "The efficacy of non-invasive brain stimulation protocols for inducing neuroplasticity." Thesis, Wansbrough, Kym (2016) The efficacy of non-invasive brain stimulation protocols for inducing neuroplasticity. Honours thesis, Murdoch University, 2016. https://researchrepository.murdoch.edu.au/id/eprint/40685/.
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Neuroplasticity refers to the brain’s ability to change with experience. Continuous theta burst stimulation (cTBS) is a non-invasive brain stimulation technique capable of temporarily inducing neuroplasticity in the primary motor cortex (M1), as indicated by changes in the excitability of the stimulated brain region. However, cTBS-induced neuroplasticity shows large inter-individual variability, which limits its potential in research and clinical settings. The present study investigated whether down-regulating motor cortical inhibition, with cTBS applied using a lower than conventional intensity (cTBSlow), is capable of making the brain more amenable to the neuroplasticity-inducing effects of cTBS applied using the conventional intensity. Thirty-two, right-handed, healthy adults participated in two experimental sessions: 1) cTBS primed by cTBSlow; 2) cTBS primed by sham stimulation. Due to unforeseen technical issues, there were two groups: group 1 received cTBSlow with conventional bursts; group 2 received cTBSlow with reduced pulses per burst. Motor cortical excitability and inhibition were measured from an intrinsic hand muscle at baseline, between the two cTBS applications, and following cTBS. In group 1, cTBSlow reduced inhibition in M1, however, there was no systematic change in motor cortical excitability following cTBS primed by cTBSlow or primed by sham. This lack of effect may be due to unreliable neuroplasticity induction in M1 following cTBS alone. In group 2, long-lasting and less variable changes in motor cortical excitability were found following an unconventional cTBS pattern. These findings confirm the variability of cTBS-induced neuroplasticity and highlight the importance of developing novel protocols to induce less variable neuroplasticity responses.
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Facchini, Silvia. "Neuroplasticity in Neuro-oncology: Neuropsychological and neuroimaging correlates of brain tumors." Doctoral thesis, Università degli studi di Padova, 2020. http://hdl.handle.net/11577/3426167.
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Brain tumors are a rare disease, however the cost in term of unfavorable prognosis and impact on quality of life is very high. The complex treatment requested by a brain tumor (surgery and pharmacological therapy) may determine neurological and cognitive consequences, that need an immediate and precise intervention. For this reason, novel diagnostic methods that combine behavioral and imaging data are requested. This research work was aimed at investigating cognitive and imaging correlates of brain tumors and is built on different aims.
The first goal was the definition of the neuropsychological profile of brain tumors. We specifically focused on cognitive deficits associated with the pathophysiology of the tumor. In other words, we investigated if brain tumors may cause a specific type of cognitive damage, based on the specific pathophysiological behavior in affecting the brain. To this end, an observational study was designed and the assessment of a cohort of brain tumor patients in the pre-operative stage was performed. By means of an extensive neuropsychological protocol, patients were evaluated in different cognitive domains. This study allows us to describe the cognitive features of the tumors, by taking into account some physiological variables: type of tumor (e.g. glioma vs meningioma), site of the lesion, extension of the lesion.
To the best of our knowledge, no study so far has defined the cognitive profile of brain tumors taking in account the specific neurological nature of this pathology, in order to define a suitable neuropsychological battery for the cognitive characterization of brain tumors. The second aim concerned precisely the effort to define the specificity of the neuropsychological battery in detecting the particular cognitive disease consequent to brain tumors. To achieve this goal, we compared the neuropsychological performance of the group of patients with brain tumor with a group of patients with focal stroke, a neurological disorder involving a very different pathophysiological process. This implies the identification of the neuropsychological tests that are sensitive in detecting the specific as well as subtle cognitive deficits consequent to brain tumors.
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The third aim had a longitudinal perspective and concerned the study of the effects of tumor resection on cognitive functions in the long term. To achieve this goal, we analyzed the behavioral data of the group of patients at three different time points: pre-surgical, post-surgical and one month follow-up. We expected a global worsening of the cognitive scores in the immediate post-operative stage, with a subsequent recovery at one month follow-up. A preliminary study was also conducted in order to define the effect of the treatment (radiotherapy and chemotherapy) on cognitive functions, with the aim to clarify the interaction of surgery and treatment in affecting the brain. Hence a further follow-up was also conducted four months from the neurosurgery and after the therapy. Importantly, this study clarified the interaction between the cognitive effects of the treatment and surgical intervention. Furthermore, it shed light on the relevance of follow-up neuropsychological assessment in monitoring brain tumors.
The present doctoral thesis aimed at clarifying the contribution of neuropsychological as well as neuroimaging measures in order to better characterize the specific pathophysiological processes beneath functional and cognitive symptoms. For this reason, a further effort consisted in exploring structural and functional neuroimaging biomarkers able to predict the patient’s quality of life after tumor surgical resection. We furthermore aimed to assess the added value of the use of local and global brain connectivity in the clinical decision process. To this end, together with the neuropsychological evaluation, metabolism and perfusion data were longitudinally acquired, using simultaneous dynamic PET and MRI techniques. These data were acquired before surgery, after one month, and after three months from surgery. This study is still ongoing.
The overarching goal in the long term of the whole research is to take into account together neuroplasticity and neuropsychological aspects in neuro-oncology in order to create a new way of taking care of patients with brain tumor. Of note, the correlation between tumor variables, behavioral outcome and structural, functional, and metabolic metrics of brain organization allows individualized planning of surgery and treatment. This planning will therefore be tailored considering the characteristics of the single patient, leading to a better outcome and a reduced impact on functions and quality of life.
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Jonckheere, Ruiz de Larrinaga Julie. "Bases moléculaires et cellulaires des effets antidépresseurs de l'électro-convulsivothérapie (ECT)." Thesis, Université Grenoble Alpes (ComUE), 2017. http://www.theses.fr/2017GREAV023/document.
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L'électroconvulsivothérapie (ECT) est une réponse thérapeutique reconnue comme efficace face à la résistance et au délai d'action des agents pharmacologiques, pour les épisodes dépressifs majeurs. Bien que l'efficacité thérapeutique des ECT soit reconnue de tous, la connaissance incomplète des effets biologiques qui sous tendent l'effet thérapeutique contribue à discréditer ce soin. Les marqueurs biologiques ne sont pas facilement accessible chez l’Homme, il a donc été développé chez les rongeurs, l’équivalent des ECT : les stimulations électro-convulsives (ECS). A ce jour, les divers résultats provenant des études chez les animaux n’ont permis d’obtenir des conclusions claires, et ceci est majoritairement dû à l’utilisation d’animaux naïfs. Dans ce contexte, l'objectif du projet de thèse était d'analyser les effets biologiques et comportementaux des ECS répétées, modèle de l'électro convulsivothérapie, sur un modèle animal de troubles psychiatriques : la souris MAP6 KO. En effet, ces souris expriment constitutivement des altérations biologiques et comportementales assimilées à certains symptômes de la dépression. Nous avons montré qu’un traitement par ECS améliore certaines des altérations comportementales des souris MAP6 KO, avec un maintien dans le temps différent selon le comportement analysé. Au niveau biologique, le traitement par ECS n’induit pas de modification détectable de l’expression des protéines dans le cerveau, mais induit une augmentation de la neurogénèse adulte hippocampal, et plus particulièrement une augmentation du taux d'intégration des neurones néoformés. L'augmentation du nombre de nouveaux neurones survivants pourrait être favorisée par l’augmentation de la complexité de l’arborisation dendritique et de la densité synaptique. De plus nous observons une augmentation de la densité des épines dendritiques dans les neurones corticaux et une augmentation de l’expression du BDNF dans l’hippocampe. En conclusion, le projet de thèse montre que les ECS appliquées aux souris MAP6 KO-ont un effet important au niveau de la plasticité cérébrale et plus particulièrement au niveau de l’intégration des nouveaux neurones issus de la neurogénèse adulte hippocampiqueIn Major depressive disorder, the electroconvulsive therapy (ECT) is recognized as an effective treatment to face drug-resistance and action latency of pharmacological agents. Although the therapeutic efficacy of ECT is internationally recognized, the ill-characterized biological effects of ECT contribute to discredit this treatment. Direct access of specific markers in human is not easy, prompting the development of the animal counterpart of ECT, the electro convulsive stimulations (ECS). To date, current results arising from ECS studies in animals remain not fully conclusive because mainly data have been obtained with unchallenged/naive animals. The objective of this project was to analyze the biological and behavioral effects of ECS treatment, on an animal model of psychiatric disorder: the MAP6-KO mice. Indeed MAP6-KO mice (also known as STOP KO mice) constitutively exhibit behavioural and biological features relevant to some aspects of major depressive disorder. We found that ECS treatment has an overall beneficial effect on several constitutive behavioural defects, displayed by MAP6 KO mice, with variable lasting times. At biological levels, ECS treatment did not induce detectable modification of brain proteins expression pattern, but induce an overall increase of hippocampal neurogenesis, and more particularly potentiate the survival rate of newborn neurons, probably through an increase dendritic complexity and dendritic spines density. We also found that ECS enhance dendritic spines density in vivo in cortical neurons and increase hippocampal levels of the trophic factor, BDNF. In summary our work provide evidence that ECS treatment when applied to MAP6 KO mice induces major neuronal plasticity events, the stronger being the increased integration rate of hippocampal new-born neurons
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Ofori, Ernest Kwesi. "EFFECT OF OPTOGENETIC STIMULATION ON NEUROPLASTICITY OF THE EMBRYONIC CHICK MOTOR SYSTEM." OpenSIUC, 2014. https://opensiuc.lib.siu.edu/theses/1458.
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There is growing knowledge that neuronal circuitry undergoes alteration throughout development. Experience plays a key role in the reorganization of neuronal circuitry through the various mechanisms of learning. For example, when an animal is deprived of sensory input such as light in one or both sides of the eye, it can result in blindness on that side. In a study of rats placed in either isolated or enriched environments, those placed in enriched environments performed better on learning tests (maze test) than those placed in isolated environment. There was increased neurogenesis, synaptogenesis, myelination and angiogenesis in rats placed in enriched environments. These were all as a result of learning, which induces neuroplasticity in the nervous system. The goals of this study were to determine how evoked movement is altered by changes in key parameters of light stimulation: intensity and period and to determine if one hour of light (optogenetic) stimulation could give rise to plastic changes in the nervous system as indicated by alterations in spontaneous motility. To ascertain how evoked motor activity influences neuronal activity through learning and experience, optogenetics was employed to evoke movement in an embryonic chick at embryonic day nine (E9) after electroporation of a channelrhodopsin variant, ChIEF, into the neural tube. I first attempted to determine the optimal intensity needed to cause neuroplasticity in an embryonic chick by varying current to a LED light to produce three different light intensities. A protocol of 5 pulses of light with a period of 2 seconds was used to illuminate the right leg of 5 embryonic chicks with each intensity. To determine the optimal period of stimulation, I varied the period to 3 s and 4 s with one animal. Stimulation for an hour with a training protocol of 1800 pulses/hour (with a period of 2 s) of blue light (470 nm) was then used to illuminate the right thigh of the embryonic chick. There were varied responses to light of all intensities used for stimulation, but high light intensity (maximum - 100%) seemed to have produced the best responses in terms of producing the largest joint angle changes and shortest latencies of movement in all joints of the leg of embryonic chick. Movements of the hip and ankle joints were the most robust. This was closely followed by those of the mid (83.33%) intensity. Therefore, it can be inferred that the greater the intensity of light, the better the response. The training protocol did not produce significant changes in embryonic activity. There were some decreases in joint angles and variable spontaneous movement duration in all animals used but there could be some changes going on at the neuronal or muscular level which were beyond the scope of this study to investigate. It is my hope that this study will provide some knowledge pertinent to the treatment or management of neurodevelopmental disorders that may result in paraplegia or Erb's palsy.
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Calvert, Dorys Faria. "L'expérience théâtrale comme expérience de transformation : théâtre et neuroscience des émotions." Thesis, Paris 3, 2014. http://www.theses.fr/2014PA030122.
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Il s’agit d’une étude interdisciplinaire – englobant essentiellement le théâtre, la psychologie et les neurosciences – dont le but est celui d’analyser le potentiel transformateur (et, d’une certaine manière, thérapeutique) inhérent à la pratique théâtrale. Ce travail se divise en deux axes centraux d’investigation : le premier se concentre sur le dialogue que le théâtre a entretenu avec les sciences de la vie au long de l’histoire de la civilisation occidentale tout en mettant en avant l’idée selon laquelle l’étude scientifique des émotions se présente comme le fil conducteur des échanges théorico-pratiques entre les arts scéniques et les sciences du vivant. Le deuxième axe de ce travail de recherche concerne les rapports entre les neurosciences contemporaines des émotions, le travail de l’acteur et les modifications que le l’expérience théâtrale peut opérer – surtout chez l’acteur – sur le plan ontologique. Dans ce travail de recherche, quelques notions neuroscientifiques qui s’avèrent fondamentales pour l’élaboration d’une approche neurobiologique du travail émotionnel de l’acteur ont été développées. Ce sont : la neuroplasticité, le système de neurones miroirs, le circuit cérébral du plaisir et l’utilisation consciente de la mémoire procéduraleThis is an interdisciplinary study – essentially encompassing theater, psychology and neuroscience – whose goal is to analyze the transforming (and, somehow, therapeutic) potential inherent to theater practice. This work is divided into two core areas of investigation: the first focuses on the dialogue that the theater has had with the life sciences throughout the history of Western civilization, highlighting the idea that the scientific study of emotions is presented as the main thread between theoretical and practical exchanges of the performing arts and life sciences. The second focus area of this research concerns the relationship between contemporary neuroscience of emotions, the work of the actor and the transformations that could occur through the theatrical experience – especially for the actor – on an ontological level. In this research, some neuroscientific concepts that prove fundamental to the development of a neurobiological approach to the emotional work of the actor have been developed. They are: neuroplasticity, the neuron mirror system, the brain gratification circuit and the conscious use of the procedural memory
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Cefis, Marina. "Impact des modalités d'un exercice physique sur la neuroplasticité. Focus sur les sources de BDNF." Thesis, Bourgogne Franche-Comté, 2019. http://www.theses.fr/2019UBFCK049/document.
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L’exercice physique (EX) est reconnu comme la stratégie non pharmacologique la plus efficace pour améliorer la santé cérébrale. Les études menées chez l’Homme et l’animal s’accordent pour impliquer le brain-derived neurotrophic factor (BDNF), une neurotrophine dont les taux cérébraux augmentent en réponse à l’EX et qui est unanimement reconnue comme une molécule de signalisation cruciale de la neuroplasticité. Principalement exprimé par les neurones, le BDNF est également très exprimé par la cellule endothéliale et la cellule musculaire. Très largement sollicités lors d’un effort physique, l’endothélium et le muscle pourraient intervenir dans les effets positifs induits par l’EX. Bien qu’il existe aujourd’hui un consensus sur l’implication du BDNF dans les effets cérébraux de l’EX, il n’en existe pas concernant les modalités d’EX à pratiquer pour optimiser de manière efficace la plasticité cérébrale. Dans ce contexte, les objectifs de ces travaux étaient de déterminer l’impact des modalités de l’EX sur les expressions protéiques de BDNF dans différents territoires (cerveau, endothélium, muscle) et d’étudier les mécanismes à l’origine de l’augmentation de BDNF en réponse à l’EX.Nos résultats montrent que 1) l’expression du BDNF dans des vaisseaux périphériques de même territoire vasculaire (diamètre interne différent) est similaire en réponse à l’EX et majoritairement d’origine endothéliale, 2) l’augmentation de l’expression cérébrale de BDNF en réponse à l’EX dépend de l’intensité de l’EX, mais pas du type de contraction (excentrique/concentrique), 3) la mémoire est restaurée par un EX de forte intensité, 4) l’EX n’impacte pas l’expression musculaire de BDNF, mais augmente l’expression du précurseur de l’irisine (FNDC5), 5) l’expression du BDNF dépend de la composition du muscle en fibres musculaires, 6) les effets cérébraux de l’intensité de l’EX ne semblent pas être reliés à la surexpression de l’irisine musculaire.En conclusion, nos données démontrent que l’EX impacte positivement l’expression endothéliale, cérébrale mais pas musculaire de BDNF. Les résultats mettent en évidence l’importance du paramètre intensité de l’EX sur les taux cérébraux de BDNF. Enfin, selon nos données obtenues, l’irisine et le BDNF musculaires ne semblent pas être impliqués dans l’augmentation cérébrale de BDNF en fonction de l’intensité de l’EXPhysical exercise (EX) is recognized as the most potent non-pharmacological strategy to positively enhance brain health. From Human and animal studies there is a consensus to involve brain-derived neurotrophic factor (BDNF), a neurotrophin strongly expressed in response to EX and implicated in neuroplasticity mechanisms. Mainly expressed by neurons, BDNF is also expressed by endothelial and muscle cells. Largely sought during a physical effort, endothelium and skeletal muscle could be involved in positive effects induced by EX. Although there is a real consensus about BDNF and cerebral effect of EX, the typology of the better regimen of EX to enhance cerebral plasticity is not known. In this context, objectives of this works were to determine the impact of EX modalities on BDNF protein expression in different territory (brain, endothelium and muscle) and to identify mechanisms related in BDNF increases in response to EX.Our results showed that 1) BDNF expression in peripheral vessels from the same vascular territory (distinct internal diameter) is similar in response to EX, 2) cerebral BDNF increases induced by EX is dependent on EX intensity but not on the type of contraction (eccentric/concentric), 3) memory is restored by high intensity EX, 4) after EX, BDNF muscular expression is unchanged while the precursor of irisine (FNDC5) expression is increased, 5) BDNF expression depends on muscular fibers typology, 6) cerebral beneficial effects of EX intensity is might not be related to muscular irisine production.In conclusion, our data demonstrated that EX positively impact endothelial, cerebral but not muscular BDNF expression. Results highlighted the importance of the intensity parameter of EX on cerebral BDNF levels. Finally, according to our data, irisine and BDNF from the muscle might not be related to the cerebral increases of BDNF induced by EX intensity
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Matamala, Gómez Marta. "The use of immersive virtual reality in neurorehabilitation and its impact in neuroplasticity." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/666826.
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This thesis aim to test the effectiveness of an immersive virtual reality set-up by using an embodied virtual body in neurorehabilitation, specifically for motor and chronic pain disorders.
More specifically, my first study entitled: Motor-cognitive training through Immersive Virtual Reality during the immobilization period in distal radius fracture patients, aims to investigate whether an upper limb immersive virtual reality (IVR) training program, may improve the motor and functional ability of a fractured arm in 54 distal radius fracture (DRF) patients during the immobilization period. With this intention, we compared 6 weeks of our IVR training group (n=20), with 6 weeks of a non-IVR training group (n=20), and with another conventional rehabilitation group (n=14), during the immobilization period. We observed that through our training program patients in the IVR training group reached a better motor-functional ability of the fractured arm after cast removal, compared to the patients in the control groups: non-immersive virtual reality group and conventional rehabilitation group. Finally, patients in the IVR training group presented better results in the follow-up (6 weeks later) compared to the control groups, especially in the wrist range of motion.
Secondly, we wanted to investigate the effects of the upper limb IVR training program in chronic stroke patients without arm mobility with a case study: Using immersive virtual reality to rehabilitate the paretic upper limb in chronic stroke patients. In that case study, we tested the IVR program in three chronic stroke patients. To this aim all three chronic stroke patients, underwent two IVR training periods during 5 weeks every day, with a 3 weeks period of pause between the two training periods. After the first training period we found improvements in motor recovery of the paretic arm, as well as in the cognitive capability and quality of life of all three chronic stroke patients. Further, we observe that the motor-cognitive improvements obtained after the first IVR training period remained over time, during the period of pause. However, the second IVR training period was not effective to further enhance motor and cognitive improvements. Further, a pre-post brain imaging analysis by using resting state and diffusor tension imaging (DTI) techniques, allowed us to identify the underpinning neuroplastic changes following the first IVR training, that were mainly found at the cerebellum from a functional connectivity point of view, and in the primary motor cortex from an structural point of view, in all three chronic stroke patients.
Finally, the last study of this thesis entitled: Immersive virtual reality reliefs pain in patients with complex regional pain syndrome type I but not with peripheral nerve injury, aimed to investigate whether varying properties of a virtual arm co-located with the real arm modulated pain ratings in patients with chronic arm/hand pain due to complex regional pain syndrome (CRPS) type I (without nerve injury) or peripheral nerve injury (PNI). CRPS (n=9) and PNI (n=10) patients were immersed in VR and the virtual arm was shown at four transparency levels (transparency test) and three sizes (size test). We evaluated pain ratings throughout the conditions and assessed the virtual experience, finding that patients with chronic pain can achieve levels of ownership and agency over a virtual arm similar to healthy participants. All seven conditions globally decreased pain ratings to half. Increasing transparency decreased pain in CRPS but did the opposite in PNI, while increasing size slightly increased pain ratings only in CRPS.
In overall my doctoral thesis pave the way to the use of embodiment through an IVR set-up in neurorehabilitation following the principles of body illusions for rehabilitation.La presente tesis pretende hacer una breve revisión de las diferentes técnicas de integración multisensorial en rehabilitación utilizando principalmente el feedback visual y que han llevado a la implementación de la realidad virtual como herramienta terapéutica. Actualmente, la realidad virtual está adquiriendo un papel importante en el campo de la rehabilitación, y en específico en el campo de la neurorehabilitación para el tratamiento de alteraciones motoras, cognitivas y síndromes dolorosos. Sin embargo, todavía es una incógnita cuál es la manera más efectiva de aplicarla y que pacientes se pueden beneficiar en mayor grado de ella. Por esta razón, en esta tesis doctoral se presentan tres diferentes estudios en los cuales se aplica el uso de un sistema de realidad virtual immersiva, generando la ilusión de posesión de un cuerpo virtual. Específicamente, el primer estudio está realizado con pacientes ortopédicos. El segundo estudio es un caso estudio realizado con tres pacientes neurológicos, y el tercer estudio está realizado con un grupo de pacientes que sufren dolor crónico neuropático. En los tres estudios, se demuestra que el hecho de generar la ilusión de posesión de un cuerpo virtual mediante el uso de un sistema de realidad virtual immersiva, permite mejorar déficits motores, cognitivos y dolorosos en diferentes patologías. Esta tesis doctoral abre el camino a la introducción de nuevas técnicas de tratamiento en el campo de la neurorehablitación mediante el uso de técnicas de integración multisensorial, como los sistemas de realidad virtual immersiva.
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Ireland, Shelley Margaret Lorraine. "The plasticity of the visual system following damage of the brachium of the superior colliculus in neonatal and adult hamsters :." Thesis, [Hong Kong : University of Hong Kong], 1991. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13204907.
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Siu, Timothy Lok Tin Medical Sciences Faculty of Medicine UNSW. "Artificial vision: feasibility of an episcleral retinal prosthesis & implications of neuroplasticity." Awarded By:University of New South Wales. Medical Sciences, 2009. http://handle.unsw.edu.au/1959.4/42879.
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Background. A visual prosthesis is a conceptual device designed to activate residual functional neurons in the visual pathway of blind individuals to produce artificial vision. Such device, when applied to stimulate the vitreous surface of the retina, has proven feasible in producing patterned light perception in blind individuals suffering from dystrophic diseases of the retina, such as aged-related macular degeneration (AMD). However the practicality of such approach has been challenged by the difficulty of surgical access and the risks of damaging the neuroretina. Positioning a visual implant over the scleral surface of the eye could present a safer alternative but this stimulation modality has not been tested in diseased retinas. Additionally, recent research has shown that the adult neocortex retains substantial plasticity following a disruption to its visual input and the potential deterioration in visual capabilities as a result of such experience modification may undermine the overall bionic rescue strategy. Methods. Two animal models mimicking the principal pathologies found in AMD, namely photoreceptor degeneration and reduced retinal ganglion cell mass, were used to evaluate the efficacy of trans-scleral stimulation of the retina by recording electrical evoked potentials in the visual cortex. The visual performance following the loss of pattern vision induced by bilateral eyelid suturing in adult mice was examined by analysing visual evoked potentials. Findings. Spatially differentiated cortical activations were obtained notwithstanding the underlying retinopathy in the experiment animals. The charge density thresholds were found to be similar to controls and below the bioelectric safety limit. After prolonged visual deprivation (weeks) in the mouse, the visual cortical responses evoked by either electrical or photic stimuli were both significantly reduced. An assessment of different visual capabilities using patterned stimuli demonstrated that whilst visual acuity and motion sensitivity were preserved, significant depression in luminance and contrast sensitivities was detected. Conclusion. Trans-scleral stimulation of the retina is a feasible approach for the development of a visual prosthesis. Following visual loss the adult brain exhibits significant experience-dependent modifications. These new insights may force a revision on the current bionic rescue strategy.
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Wilson, Edward. "Investigating signal cascades promoting activity-dependent neuroplasticity in monkey primary visual cortex." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=106492.
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The primate visual system represents an ideal model for the study of neural development and activity-dependent neuroplasticity. The final disposition of the visual cortex is based on a genetically determined cellular organization programmed to become influenced by the animal's environment during a critical period in early postnatal development. Thus neural connections are shaped by the sensory experience of the animal. This plasticity of the visual system declines after the closure of the critical window, and while plasticity is still present in mature animals, its strength is greatly diminished. Cortical plasticity can be restored after the closure of the critical period, however, by altering the incoming neural activity to which the network has adapted. For example, preventing light information from reaching the visual system prompts cortical reorganization in infant and adult primates, such that deprived neurons become responsive to input to the open eye. The transcription factor cyclic-AMP response element-binding protein (CREB) is implicated in cellular processes requiring remodeling of cortical circuits. In fact, CREB uses self-directed mechanisms creating functional circuits by responding to fluctuations in neural activity. For this reason, it is not unexpected for CREB to be implicated in the ocular dominance (OD) plasticity that occurs in monkey primary visual cortex following monocular enucleation (ME). Specifically, level of activated CREB (with specific phosphorylation to serine-133) is elevated in response to changes in neural activity in both activity-deprived and non-deprived visual areas. A problem with this observation, unfortunately, is that it fails to explain how CREB can produce a shift in ocular dominance in deprived neurons while those non-deprived neurons undergo no remodeling.New experimental results presented here show a region-specific alteration in the amount of inhibited CREB occurring in response to ME. Additionally, it was found that signal from the critical CREB transcriptional cofactor, TORC1, is restored to a near critical period level in adults after ME. Inhibited CREB was found to increase in deprived regions, while TORC1 increased in non-deprived regions. Taken together, these results raise the possibility that a) differential modulation of CREB residues and cofactor activation may contribute to its ability to produce output that is context specific; and b) OD plasticity requires the imbalance of CREB activation such that CREB is potentiated in the non-deprived ODCs relative to deprived-eye counterparts.Le système visuel du primate constitue un modèle idéal pour l'étude du développement neuronal et de la neuroplasticité dépendante de l'activité. L'organisation finale du cortex visuel est basée sur une organisation cellulaire génétiquement déterminée, programmée pour être influencée par l'environnement de l'animal pendant une période critique du développement post-natal.Ainsi, les connections neuronales sont formées par l'expérience sensorielle de l'animal. La plasticité du système visuel décline après la fin de cette période critique et, bien qu'existante chez les animaux matures, elle est grandement diminuée. Par contre, la plasticité corticale peut être rétablie après la fin de la période critique en altérant l'activité neuronale entrante à laquelle le système s'est adapté. Par exemple, empêcher que l'information reliée à la lumière se rende au système visuel provoque la réorganisation corticale chez les primates en bas âge et adultes, de façon à ce que les neurones privées deviennent réceptives aux entrées provenant de l'œil ouvert.Le facteur de transcription CREB (cAMP Response Element-Binding) contribue aux fonctions cellulaires requises pour le remodelage des circuits corticaux. En fait, en répondant aux variations de l'activité neuronale, CREB utilise des mécanismes autodirigés pour créer des circuits fonctionnels. Pour cette raison, il n'est pas surprenant que CREB soit impliqué dans la plasticité reliée à la dominance oculaire (DO) qui se produit dans le cortex visuel primaire à la suite de l'inactivation monoculaire (IM). Précisément, les niveaux de la forme activée de CREB (phosphorylée au site serine-133) sont élevés en réponse aux changements d'activité neuronale à la fois dans les zones visuelles privées et non privées des entrées provenant de l'oeil. Le problème relié à cette observation est le fait qu'elle n'explique pas pourquoi CREB peut induire un changement de la dominance oculaire chez les neurones privées alors que celles non privées ne sont pas remodelées.Les nouveaux résultats expérimentaux présentés ici démontrent des changements au niveau de la quantité de CREB inhibé suite à l'IM qui sont spécifiques aux zones. De plus, il a été démontré que le signal du cofacteur transcriptionnel critique de CREB, TORC1, est rétabli à un niveau comparable à celui de la période critique chez les adultes après l'IM. Le CREB inhibé était augmenté dans les zones privées, alors que TORC1 était augmenté dans les zones non privées. Ensembles, ces résultats suggèrent que a) la modulation différentielle des résidus de CREB et l'activation de ses cofacteurs pourraient contribuer à son habileté à produire des effets dépendants du contexte et b) la plasticité reliée à la DO nécessite le déséquilibre de l'activation de CREB de façon à ce que CREB est potentialisé dans les zones non-privées comparées aux zones privées.
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Reay, Riaan. "The effects of sildenafil on neuroplasticity in human neuroblastoma cells / Riaan Reay." Thesis, North-West University, 2010. http://hdl.handle.net/10394/4903.
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The antidepressant treatment of depression, currently the most debilitating psychiatric disorder, is plagued by delayed onset of action, troublesome side-effects and treatment resistance. However, a comprehensive understanding of the biological basis and treatment of depression remains elusive, prompting extensive ongoing research. The neuroplasticity hypothesis of depression has gained support from various lines of experimental and clinical evidence, whereas chronic antidepressant treatments reverse impaired neuroplasticity. The NO/cGMP pathway is believed to play an important role in the dysregulated neuroplasticity and has been a target for novel antidepressant strategies. Our laboratory recently demonstrated antidepressant-like effects of the phosphodiesterase type 5 (POE5) inhibitor sildenafil when combined with the antimuscarinic drug atropine in rats. Unpublished data suggested that sildenafil may up-regulate genes encoding for the expression of anti-apoptotic proteins in vitro. Therefore, the primary study objective was to investigate the effects of POE5 inhibitors and other modulators of the NO/cGMP pathway on neuroplasticity.
The human neuroblastoma (SH-SY5Y) and non-neuronal Chinese hamster ovary (CHO-K1) cell lines were subjected to various biological stressors associated with the neuropathology of major depression, including glutamate-induced excitotoxicity, H2O2-induced oxidative stress and serum deprivation. The latter was selected as optimal stressor in SH-SY5Y cells whereafter they were incubated for 24 hours with the antidepressat drugs imipramine, f1uoxetine and tianeptine, the mood stabilizer lithium, the POE5 inhibitors sildenafil and tadalafil, the POE4 inhibitor, rolipram and the cGMP analogue db-cGMP under conditions of serum deprivation. Also, the incubation with sildenafil and db-cGMP was performed with and without the soluble guanylate cyclase inhibitor (ODQ) or the protein kinase G (PKG) inhibitor (RP-PETcGMPS). Thereafter cell viability was measured with the MTT-and Trypan blue assays and ONA repair capacity was measured with the comet assay.
The results indicated that sildenafil exerts a protective effect against oxidative stress, as measured in the MTT assay. This property was shared by lithium, but not by db-cGMP or the antidepressants. In addition, ODQ and RP-PET-cGMPS reversed the protective effect of sildenafil, but with ODQ having a significantly greater effect. Results from the comet assay indicate that all antidepressant drugs, PDE inhibitors and db-cGMP significantly increased DNA repair capacity of SH-SY5Y cells. ODQ and RP-PET-cGMPS reversed the enhancing effects of sildenafil and db-cGMP on DNA repair capacity.
Main conclusions are that 24 hour serum deprivation of human neuroblastoma (SHSY5Y) cells provides a suitable in vitro biological stressor. Serum deprivation in combination with DNA repair capacity as biological marker of oxidative stress, exhibit appropriate predictive validity in evaluating the effects of antidepressant drugs on neuroplasticity.. Sildenafil, but not tadalafil, may possess a unique protective property against oxidative stress to increase mitochondrial function, not shared by classical antidepressants. PDE5 inhibitors share the protective property of classical antidepressants to enhance DNA repair capacity under conditions of oxidative stress. The mechanism whereby the PDE5 inhibitors exert their protective property to enhance DNA repair capacity, involve increasing levels of cGMP and is PKG mediated.
Finally, this study suggests that neuroprotective effects may contribute to the antidepressant-like activity of PDE5 inhibitors as observed in animal studies.Thesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2010.
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Sturdy, Elliot. "The Administration of the Flesh : The discourse of self-improvement and neuroplasticity." Thesis, Stockholms universitet, Institutionen för etnologi, religionshistoria och genusvetenskap, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-145383.
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This study looks at the discourse of four books that use neuroplasticity as a basis for their project of self-improvement. By using the genealogical techniques developed by Michel Foucault this study focuses upon the process of subjectivization and the techniques employed by the discourse. In particular it focuses upon the relationship between the mind and brain that is formed by the discourse.
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ANDRENELLI, ELISA. "Advanced technologies enhance exercise effectiveness in neurodegenerative disorders: evidence from neuroplasticity studies." Doctoral thesis, Università Politecnica delle Marche, 2019. http://hdl.handle.net/11566/263447.
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Le malattie neurodegenerative come la Malattia di Parkinson e la Sclerosi Multipla sono caratterizzate dalla comparsa di cellule microgliali e astrogliali reattive, un processo noto come neuroinfiammazione. L'attivazione delle cellule gliali può indurre un aumento dei livelli di citochine pro- e antinfiammatorie e di ossigeno reattivo, che può portare alla modulazione della funzione neuronale e della neurotossicità osservata in diverse patologie neurologiche. Non ci sono prove conclusive che possano classificare l'infiammazione come una causa o una conseguenza dell'insorgenza della malattia. Tuttavia, approcci terapeutici specificamente mirati alla neuroinfiammazione e alla neuroplasticità possono rappresentare una strategia efficace per interferire con la progressione della malattia e di conseguenza per prevenire o trattare i sintomi correlati. È noto che l'esercizio fisico moduli efficacemente l'infiammazione e aumenti la plasticità sinaptica influenzando direttamente la struttura sinaptica e indirettamente rafforzando i sistemi sottostanti di supporto ad essa tra cui la neurogenesi, il metabolismo e la funzione vascolare. Sono necessari ulteriori studi per chiarire i parametri dell’esercizio necessari per modulare infiammazione e neuroplasticità, come l‘intensità, la durata, la frequenza e il tipo (aerobico o task oriented) di esercizio. Negli studi seguenti abbiamo dimostrato come un allenamento specifico dell'andatura potrebbe migliorare i sintomi che non rispondono o che rispondono scarsamente al trattamento farmacologico in due comuni disordini neurodegenerativi, la malattia di Parkinson e la sclerosi multipla. Tutti i pazienti arruolati, sia affetti da malattia di Parkinson che da sclerosi multipla, alla valutazione basale hanno mostrato un’alterata neuroplasticità che in entrambi gli studi si è ripristinata solo dopo training del cammino con robot. Questo dato neurofisiologico si è tradotto nel miglioramento clinico del freezing del cammino nella malattia di Parkinson e del cammino ed equilibrio nella sclerosi multipla.Neurodegenerative diseases such as Parkinson’s disease and multiple sclerosis are characterised by the appearance of reactive microglial and astroglial cells, a process referred to as neuroinflammation. Activation of glia cells can induce an increase in the levels of pro- and antiinflammatory cytokines and reactive oxygen species, which can lead to the modulation of neuronal function and neurotoxicity observed in several brain pathologies. There is no conclusive evidence that can classify the inflammation as a cause or a consequence of the disease onset. However, therapeutic approaches specifically targeting neuroinflammation and neuroplasticity may represent an effective strategy to interfere with the disease progression and consequently for preventing or treating the related symptoms. Exercise is known to effectively modulate inflammation and has been reported to change the inflammatory state to become anti-inflammatory or neuroprotective. Moreover, exercise increases synaptic plasticity by directly affecting synaptic structure and potentiating synaptic strength, and indirectly by strengthening the underlying systems that support plasticity including neurogenesis, metabolism and vascular function. More studies are needed to elucidate the likely range of intensity, duration, frequency, and type (aerobic or task oriented) of exercise that is required to induce such important target responses. In the following studies we showed how specific gait training could improve symptoms that are unresponsive or that poorly respond to pharmacological treatment in two common neurodegenerative disorders, Parkinson's disease and multiple sclerosis. At baseline assessment, all patients enrolled, either suffering from Parkinson's disease or multiple sclerosis, showed an impaired neuroplasticity that recovered only after robot gait training. This neurophysiological result was correlated to clinical improvement of the freezing of gait in Parkinson's disease and gait and balance in multiple sclerosis.
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Traini, Enea. "Cholinergic enhancing strategies and brain neuroplasticity. From preclinical evidence to clinical applications." Doctoral thesis, Università di Catania, 2015. http://hdl.handle.net/10761/4076.
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Cholinergic precursors have represented the first approach to counter cognitive impairment occurring in adultonset dementia disorders. In preclinical studies choline alphoscerate increases the release of acetylcholine in rat hippocampus, facilitates learning and memory in experimental animals, improves brain transduction mechanisms and decreases age-dependent structural changes occurring in rat brain areas involved in learning and memory. The compound exerts neuroprotective effects in models of altered cholinergic neurotransmission and of brain vascular injury. Some of our studies have also shown that combination of ChE-Is and the cholinergic precursor choline alphoscerate increases brain acetylcholine levels more effectively than single compounds alone. In clinical studies choline alphoscerate improved memory and attention impairment, as well as affective and somatic symptoms in dementia disorders. ASCOMALVA (Effect of association between a ChE-I and choline alphoscerate on cognitive deficits in AD associated with cerebrovascular injury) is a double-blind trial investigating if the ChE-I donepezil and choline alphoscerate in combination are more effective that donepezil alone. Over the 24-month observation period, patients of the reference group showed a moderate time-dependent worsening in all the parameters investigated. Treatment with donepezil plus choline alphoscerate significantly slowed changes of the in cognitive and functional items and an improvement in behavioural parameters, mainly apathy, superior to that induced by donepezil alone. It is suggested that this association may represent a therapeutic option to prolong beneficial effects of cholinergic therapies in Alzheimer's disease patients with concomitant ischemic cerebrovascular disorders. In summary, choline alphoscerate has significant effects on cognitive function with a good safety profile and tolerability. Although limited both in terms of size of the samples investigated and of the length of treatment, preclinical and clinical results presented suggest that cognitive enhancing capabilities of choline alphoscerate merit of being further investigated in appropriate trials.
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Baum, David. "Dimorphismes sexuels de la neuroplasticité respiratoire associée au syndrome d'apnées obstructives du sommeil et caractérisation d'un nouveau modèle murin." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS044/document.
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Le syndrome d’apnées obstructives du sommeil (SAOS) se caractérise par des collapsus récurrents des voies aériennes supérieures pendant le sommeil, entraînant des épisodes d’hypoxie/hypercapnie. Par ces variations gazeuses, le SAOS entraîne des altérations cardiorespiratoires, représentant ainsi un danger de vie pour les patients, mais dont certaines sont moins marquées chez les patientes. La prévalence chez les hommes est plus élevée que celle des femmes pré-ménopausées et elle est augmentée par l’obésité.L’objectif de ce doctorat était de caractériser les dimorphismes sexuels dans la neuroplasticité associée au SAOS, à l’origine des altérations cardiorespiratoires. Pour cela, nous avons soumis des souris à un protocole d’hypoxie intermittente chronique (HIC), ce modèle récapitulant l’hypoxie récurrente du SAOS. Dans l’encéphale de ces souris, nous avons pu apprécier des atteintes différentielles entre les souris mâles et femelles au sein de structures cardiorespiratoires avec un profil de neuroplasticité réservé aux femelles qui pourrait atténuer chez ces dernières les effets de l’HIC. Cela ouvre des pistes explicatives des différences sexuelles retrouvées chez les patients et patientes SAOS. Nous avons également caractérisé une souche de souris obèses (New Zealand Obese) en tant que modèle du SAOS. Nous fournissons ainsi le premier modèle murin naturel du SAOS lié à l’obésité. Enfin, ce travail contribue à une meilleure connaissance des différences sexuelles observées dans le SAOS et fournit un modèle facilement accessible qui offre la possibilité de réaliser des études plus complètes de la pathologie du SAOSThe obstructive sleep apnea syndrome (OSAS) is characterized by recurrent collapse of the upper airways during sleep, generating episodes of hypoxia/hypercapnia. Thus, OSAS leads to life-threatening cardiorespiratory comorbidities, but of which some are less severe in female patients. The prevalence in men is higher than that of pre-menopausal women and it is increased by obesity. This doctoral thesis aimed to characterize sex differences in the neuroplasticity related to cardi-orespiratory comorbidities found in OSAS. In this context, we submitted mice to a protocol of chronic intermittent hypoxia, a model that recapitulates episodic hypoxia of OSAS. On isolated brain sections, we observed differential implication of cardiorespiratory structures between male and female mice with a specific neuroplastic pattern in females that could possibly explain sex differences observed in OSAS patients. In parallel, we have characterized an obese mouse strain (New Zealand Obese) as a model of OSAS. Thus, we provide the first naturel mouse model for OSAS related to obesity. The work presented in this thesis provides better understanding of sex differences observed in OSAS and provides a new model of OSAS that should allow more complete studies of the pathology of OSAS
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Bosnyak, Daniel J. Roberts L. E. "Mechanisms and dynamics of the human auditory steady-state response /." *McMaster only, 2003.
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Yuen, Sung-lai. "Plasticity of human brain networks as revealed by functional magnetic resonance imaging." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38837602.
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Alspector, Emily Bitler Elizabeth. "The relationship between neurogenesis and pain behavior." Diss., Connect to the thesis, 2008. http://hdl.handle.net/10066/1325.
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Harrison, Elaine. "Morphological correlates of synaptic plasticity after long term potentiation in the rat hippocampus." n.p, 2000. http://library7.open.ac.uk/abstracts/page.php?thesisid=44.
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Rakai, Brooke D., and University of Lethbridge Faculty of Arts and Science. "Experience dependent plasticity of stroke outcome." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Neuroscience, c2008, 2008. http://hdl.handle.net/10133/2518.
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Stroke outcome is highly variable. Experiments in this thesis test the hypothesis that experience prior to a stroke is an important variable in the manifestation of stroke. Optokinetic tracking was used to evaluate the effects of visual cortex stroke and MCA occlusion in rats. Normal laboratory rats showed a small, but significant decrease in tracking thresholds following visual cortex stroke. Animals with developmental visuomotor experience or reach training experience in adulthood, however, had tracking thresholds which were substantially increased, and the effects of visual cortex strokes were greater. MCA occlusions did not affect tracking behaviour. These data indicate that specific experiences engage neural plasticity that can alter brain function. These changes can, in turn, affect the behavioural manifestation of a stroke. Understanding the effect that environmental experience has on stroke outcome promises to enable better characterization of strokes, and set appropriate behavioural baselines for the measurement of recovery of function.vi, 135 p. : ill. ; 29 cm