Models of catastrophic cortical plasticity contributing

灾难性皮质可塑性贡献模型

• 批准号: 6588521
• 负责人: MICHAEL M MERZENICH
• 金额: $ 17.38万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-05-01 至 2007-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6588521
• 关键词: Aotus; auditory cortex; behavior test; behavioral /social science research tag; brain mapping; developmental disease /disorder; disease /disorder model; dystonia; electrophysiology; experience; laboratory rat; learning; method development; motor cortex; nervous system disorder; neural information processing; neural plasticity; neuromuscular disorder; neurons; neuropathology; neuropsychology; psychomotor function; sensorimotor system; sensory cortex; sensory feedback; somesthetic sensory cortex; speech

The overall objective of this project is to determine specific ways in which learning-induced changes in cortical representations contribute to the origins of and the expressions of acquired and developmental movement disorders and severe disorders of language, and to use that understanding as a source of insight for defining the forms of new neuroscience-based therapies designed to remediate them. We shall further develop and elaborate models of origin of a) focal dystonias of the hand (fDh); b) the usually-severe language disorder component of pervasive developmental disorders (PDDs); and c) some forms of generalized developmental dystonia and cerebral generate representations of learned stimuli and behaviors. It has already contributed to a growing appreciation of what postnatal functional self-organizing mechanisms contribute to human performance ability and disability and to the specific mechanisms that underlie these cortical cellular, synaptic and circuit changes process. Our principal focus is directed toward creating special models of "catastrophic plasticity" that have human neuropathology parallels. It is hypothesized that catastrophic cortical plasticity underlies the emergence of acquired movement disorders and repetitive strain injury symptoms in adults, and accounts for some of the major deficits of pervasive developmental disorders, developmental generalized dystonias and some forms of cerebral palsy. A more complete understanding of the neurological origins of the deficits contributed by the progressive learning in a defectively functionally self- organizing brains will provide crucial insights into possible forms of a new class of remediative training strategies and our understanding the physiological impacts of brain trauma, oxygen deprivation, or inherited weaknesses that contribute-along with learning to the origins of these severely disabling conditions. The continuation experiments are designed to deepen our understanding of the complex neurological origins of these common human maladies, and to provide us with information that will guide the development of remedial training strategies that could allow us to more effectively help many of these severely impaired individuals.

本项目的总体目标是确定学习诱导的皮质表征变化如何有助于后天和发育性运动障碍和严重语言障碍的起源和表达，并将这种理解作为洞察的来源，以确定旨在补救这些疾病的基于神经科学的新疗法的形式。我们将进一步发展和阐述a)手局灶性肌张力障碍(FDH)的起源模型；b)广泛性发育障碍(PDDS)通常严重的语言障碍成分；以及c)某些形式的广泛性肌张力障碍和大脑产生习得刺激和行为的表征。它已经帮助人们越来越多地认识到出生后功能性自组织机制对人类行为能力和残疾的贡献，以及这些皮层细胞、突触和回路变化过程中的特定机制。我们的主要关注点是建立与人类神经病理学相似的“灾难性可塑性”的特殊模型。据推测，灾难性的皮质可塑性是成人后天运动障碍和重复性劳损症状出现的基础，也是广泛性发育障碍、发育性全身性肌张力障碍和某些形式的脑性瘫痪的主要缺陷的原因。更全面地了解功能有缺陷的自组织大脑中渐进学习造成的缺陷的神经学根源，将为一类新的补救训练策略的可能形式提供关键的见解，并有助于我们理解大脑创伤、缺氧或遗传性弱点的生理影响-以及学习导致这些严重残疾疾病的起源。继续实验的目的是加深我们对这些常见人类疾病的复杂神经起源的理解，并为我们提供信息，指导制定补救训练策略，使我们能够更有效地帮助许多这些严重受损的人。