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Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2007. / Härtill 4 uppsatser.

Diss. (sammanfattning) Uppsala : Univ., 2002. / Härtill 6 uppsatser.

Dissertation (Ph.D.)--University of South Florida, 2006. / Includes bibliographical references (leaves 126-136). Also available online.

Orientador: Li Li Min / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas / Made available in DSpace on 2018-08-10T03:39:21Z (GMT). No. of bitstreams: 1 Cannonieri_GiannaCarla_M.pdf: 2892396 bytes, checksum: 985d7c525864a8b128f7d574556ef6b9 (MD5) Previous issue date: 2007 / Resumo: Introdução: O treinamento prolongado de tarefas motoras está associado com a execução automática dos movimentos. A adaptação funcional induzida pelo treinando resulta em uma melhora do desempenho motor. Não se compreende ainda inteiramente se essa adaptação funcional é refletida em mudanças plásticas na estrutura do cérebro. Objetivo: Investigar a presença e o grau de plasticidade cerebral estrutural do cérebro induzida por um treino motor bimanual prolongado em digitadores experientes profissionais. Sujeitos/Métodos: Foram avaliados 17 digitadores profissionais. Através da técnica de Mofometria Baseada em Voxels (VBM), que utiliza imagens de ressonância magnética de alta resolução, correlacionamos o tempo de prática como digitador com o volume de substancia cinzenta cerebral (VSC). Utilizamos as regiões de interesse (ROI) disponibilizadas pela AAL (anatomical automatic labeling) library e o programa MARSBAR para o SPM2. Resultados: Encontramos uma regressão positiva significativa entre VSC e tempo de prática em seis regiões cerebrais: hemisfério cerebelar inferior medial esquerdo, hemisfério cerebelar inferior medial direito, região frontal orbital medial direita, lóbulo paracentral direito e o pólo temporal direito. Discussão: Nosso estudo sugere que a prática prolongada de digitação pode produzir mudanças macroscópicas estruturais no cérebro de adultos saudáveis. Uma atividade motora coordenada, bimanual e seqüencial dos dedos impõe uma demanda neural nas regiões corticais relacionadas à programação e execução da tarefa motora, incluindo a área motora suplementar, córtex pré-frontal e cerebelo. Conclusão: A plasticidade cerebral pode ocorrer am adultos. O treino motor prolongado pode aumentar o VSC em áreas específicas do córtex cerebral e cerebelo, relacionadas à coordenação e planejamento motor, importantes para a execução da atividade de digitação / Abstract: Background: Long-term training of specific motor tasks is associated with automatic execution of movements. Functional adaptation induced by training results in performance improvement. It is not yet fully understood whether functional adaptation is reflected by plasticity changes in brain structure. Objectives: We aimed to investigate the presence and degree of structural brain plasticity induced by long-term bimanual motor activity executed by professional typists. Subjects/Methods: We studied 17 right-handed professional typists. Using voxel-based morphometry (VBM), we correlated duration of practice and gray matter volume. Local regions of interest (ROI) -VBM was applied using predefined 116 previously segmented brain sites (from the anatomical automatic labeling library) and MARSBAR package. Results: We found a significant positive regression between GMV and duration of practice in six regions: left medial inferior cerebellar hemisphere, right medial inferior cerebellar hemisphere, right medial orbital region, right paracentral lobule and the right temporal pole. Discussion: Our study suggests that long-term typewriting practice may yield macroscopic changes in brain structures of healthy adults. Non-mirror sequential bimanual finger activity coordination creates a demand in cortical regions related to the programming of motor task, including the supplementary motor area, prefrontal cortices and cerebellum. Conclusion: Neural plasticity occurs in adult brain. Long-term bimanual training may increase GMV in specific brain areas of cerebral cortex and cerebellum. These regions are related to bimanual motor coordination and planning, which are important for typing / Mestrado / Neurociencias / Mestre em Fisiopatologia Médica

Modifications of perineuronal nets to regulate plasticity Heleen Merel van 't Spijker Perineuronal nets (PNNs) are macromolecular structures formed by neurons after closure of critical periods of plasticity. During development, the central nervous system (CNS) goes through critical periods of plasticity; a period when substantial changes occur to adapt to the environment, during which many synapses are formed and also discarded. When a region of the CNS has finished its development and reached an efficient neuronal circuit, the capacity for plasticity needs to be reduced to preserve the formed circuit. PNNs are formed around neurons during this period of reduced plasticity. PNNs consist of a backbone of hyaluronan, bound by chondroitin sulfate proteoglycans (CSPGs). Here, I present my studies on the possible modifications of PNNs to regulate plasticity. Firstly, I have investigated the potential use of 4-methylumbelliferone (4-MU) to reduce PNN formation in vivo. 4-MU reduces the formation of hyaluronan. Since hyaluronan is the backbone of PNNs, I hypothesized 4-MU treatment would reduce PNN formation. For this study, I developed a method to orally administer 4-MU to rats. Subsequently, I investigated whether 4-MU treatment can improve recovery of rats after spinal cord injury, both with behavioural tests and with immunohistochemistry. Secondly, I have investigated a new binding partner of PNNs, neuronal pentraxin 2 (Nptx2). Nptx2 is secreted by neurons and regulates AMPA receptor diffusion. Nptx2 knockout mice show a prolonged critical period of plasticity in the visual cortex. Here, I have identified Nptx2 as a new binding partner of PNNs. Nptx2 is found in isolated PNN protein preparations and is removed from the surface of neurons by digestion of PNNs with chondroitinase ABC. I also determined Nptx2 facilitates PNN formation in vitro. Addition of Nptx2 to the medium of cortical neurons leads to an increase of neurons that start to form PNNs, as well as an increase in size and density of PNNs. These findings indicate Nptx2 may be used as a modulator of PNNs. Thirdly, I investigated the interaction between Nptx2 and PNNs. I developed a sandwich ELISA to determine which glycan chains from PNNs bind to Nptx2. Nptx2 binds to chondroitin sulfate E and hyaluronan. To investigate the binding properties of Nptx2, I performed quartz crystal microbalance with dissipation monitoring for Nptx2 films. Furthermore, I developed crystals of purified Nptx2 and hyaluronan for x-ray crystallography. The here presented results provide new insights in potential approaches to modulate PNN formation. Both lines of research provide a further understanding of the factors which regulate PNNs and may allow for the development of treatments for PNN related disorders.

Thesis (M.S.)--West Virginia University, 2001. / Title from document title page. Document formatted into pages; contains vii, 79 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 70-78).

Spinal cord injury (SCI) results in a number of devastating consequences, including loss of motor function, paralysis, and neuropathic pain. Concomitant peripheral tissue injury below the lesion site can result in uncontrollable nociception that sensitizes spinal neurons and promotes chronic pain. Additionally, drugs like morphine, though critical for pain management, elicit pro-inflammatory effects that exacerbate chronic pain symptoms. Currently, there is a lack of effective therapeutic mechanisms to promote regeneration at the lesion site, and a limited understanding of regulatory mechanisms that can be utilized to therapeutically manipulate spinal cord plasticity. MicroRNAs (miRNAs) constitute novel targets for therapeutic intervention to both promote repair and regeneration, and mitigate maladaptive plasticity that leads to neuropathic pain. Microarray and qRT-PCR comparisons of contused and sham rat spinal cords at 4 and 14 days following SCI indicated that a total of 35 miRNAs were dysregulated, with miR1, miR124, and miR129 exhibiting significant down-regulation after SCI, and both miR21 and miR146a being transiently induced. Localized expression of miRNAs and cellular markers indicated that changes in miRNA regulation favor the emergence of neural stem cell niches and reversion of surviving neurons to a pre-neuronal phenotype. Additionally, both uncontrollable nociception and morphine administration resulted in further dysregulation of SCI-sensitive miRNAs, along with their mRNA targets. Morphine administration significantly induced expression of both miR21 and IL6R expression, indicating that morphine-induced miRNA dysregulation is involved in the promotion of neuroinflammation that drives increased pain-sensitivity. Similarly, uncontrollable nociception significantly modulates expression of miR124, miR129, and miR146a, which inhibit cell cycle proteins and microglial activation, and dysregulation of these miRNAs, along with BDNF and IGF-1, likely contributes towards promotion of hypersensitivity in spinal neurons that underlies neuropathic pain. Consequently, SCI- sensitive miRNAs may constitute therapeutic targets for modulation of neuroinflammation and microglial activation in order to mitigate secondary injury, promote regeneration, and prevent maladaptive plasticity that drives neuropathic pain and exacerbation of chronic pain symptoms by morphine administration.

Dissertation Thesis (Ph.D.)--University of South Florida, 2007. / Title from PDF of title page. Document formatted into pages; contains 202 pages. Includes vita. Includes bibliographical references.

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 4 uppsatser.