Use Dependent Plasticity of Spinal Inhibition

使用脊髓抑制的依赖性可塑性

基本信息

  • 批准号:
    6625658
  • 负责人:
  • 金额:
    $ 35.98万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2002
  • 资助国家:
    美国
  • 起止时间:
    2002-04-15 至 2007-03-31
  • 项目状态:
    已结题

项目摘要

Both experimental animals and humans can regain the ability to stand or to step after a complete spinal cord transection. The ability to execute these tasks depends on specific training regimens, illustrating the importance of motor leading in the spinal cord. Low-thoracic transection and subsequent training leads to a persistent increase in the total inhibitory capacity of the lumbar spinal cord, exhibited by increases in GAD67, a GABA-synthesizing enzyme, and its mRNA, as well as in the alpha-1 subunit of glycine receptor and in gephyrin, a protein associated with glycine receptors. However, repetitive hindlimb training, such as stepping, returns the levels of GAD67 and glycine receptors towards normal. The central hypothesis of this proposal is that task-specific, repetitive training selectively modulates the inhibition within sensorimotor pathways associated with the execution of that task. Using a robotic device, we will test this hypothesis with a well-defined standing task in neonatally transected (T12-13) rats. Stand training allows us to compare training-induced changes in neurons associated with plantarflexion (facilitation of the soleus motor pool) and neurons associated with dorsiflexion (inhibition of the tibialis anterior motor pool). We will test three hypotheses: (1) that stand training decreases the inhibitory capacity of specific neurons associated with the ankle dorsiflexor (tibialis anterior); (2) that training selectively alters the ratio of inhibitory and excitatory synapses on the somata of individual motoneurons in motor pools associated with soleus, and (3) that pharmacologically induced changes in motor performance of spinally transected rats reflect these alterations in GABAergic and glycinergic inhibition in plantarflexion- and dorsiflexor-associated neurons as noted in the first two hypotheses. A major innovation in this work is the ability to train motor tasks, and to quantify the kinematics of standing and stepping using a newly developed robotic device. This device will allow us to impose strictly repetitive training and to assess the progress of individual animals with great precision. The proposed studies address the anatomical and molecular bases of the plasticity that may underlie rehabilitative training after spinal injury. This work will lead to better ways of testing the effectiveness of alternative training strategies and associated pharmacological interventions.
脊髓完全横断后,实验动物和人类都可以恢复站立或行走的能力。执行这些任务的能力取决于具体的训练方案,这说明了脊髓运动引导的重要性。低位胸椎横断和随后的训练导致腰脊髓的总抑制能力持续增加,表现为 GAD67(一种 GABA 合成酶)及其 mRNA、以及甘氨酸受体的 α-1 亚基和 gephyrin(一种与甘氨酸受体相关的蛋白质)的增加。然而,重复的后肢训练(例如迈步)可以使 GAD67 和甘氨酸受体的水平恢复正常。该提议的中心假设是,特定任务的重复训练选择性地调节与该任务执行相关的感觉运动通路内的抑制。我们将使用机器人设备,在新生横切大鼠 (T12-13) 中通过明确的站立任务来检验这一假设。站立训练使我们能够比较训练引起的与跖屈(促进比目鱼肌运动池)相关的神经元和与背屈(抑制胫骨前运动池)相关的神经元的变化。我们将测试三个假设:(1)站立训练会降低与踝背屈肌(胫骨前肌)相关的特定神经元的抑制能力; (2) 训练选择性地改变与比目鱼肌相关的运动池中单个运动神经元体细胞的抑制性和兴奋性突触的比例,(3) 药物诱导的脊髓横断大鼠运动性能的变化反映了跖屈和背屈肌相关神经元中 GABA 能和甘氨酸能抑制的变化,如前两个假设所述。这项工作的一项重大创新是能够训练运动任务,并使用新开发的机器人设备量化站立和行走的运动学。该设备将使我们能够进行严格的重复训练,并非常精确地评估个体动物的进展。拟议的研究探讨了可塑性的解剖学和分子基础,这可能是脊柱损伤后康复训练的基础。这项工作将带来更好的方法来测试替代训练策略和相关药理学干预措施的有效性。

项目成果

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{{ truncateString('ALLAN J TOBIN', 18)}}的其他基金

Use Dependent Plasticity of Spinal Inhibition
使用脊髓抑制的依赖性可塑性
  • 批准号:
    6477871
  • 财政年份:
    2002
  • 资助金额:
    $ 35.98万
  • 项目类别:
CELLULAR PATHOGENIC MECHANISMS IN HUNTINGTON'S DISEASE
亨廷顿病的细胞致病机制
  • 批准号:
    6494939
  • 财政年份:
    2001
  • 资助金额:
    $ 35.98万
  • 项目类别:
CELLULAR PATHOGENIC MECHANISMS IN HUNTINGTON'S DISEASE
亨廷顿病的细胞致病机制
  • 批准号:
    6287477
  • 财政年份:
    2001
  • 资助金额:
    $ 35.98万
  • 项目类别:
CELLULAR PATHOGENIC MECHANISMS IN HUNTINGTON'S DISEASE
亨廷顿病的细胞致病机制
  • 批准号:
    6490960
  • 财政年份:
    2001
  • 资助金额:
    $ 35.98万
  • 项目类别:
CELLULAR PATHOGENIC MECHANISMS IN HUNTINGTON'S DISEASE
亨廷顿病的细胞致病机制
  • 批准号:
    6627686
  • 财政年份:
    2001
  • 资助金额:
    $ 35.98万
  • 项目类别:
Core--Molecular biology
核心--分子生物学
  • 批准号:
    6478899
  • 财政年份:
    2001
  • 资助金额:
    $ 35.98万
  • 项目类别:
Core--Molecular biology
核心--分子生物学
  • 批准号:
    6326025
  • 财政年份:
    2000
  • 资助金额:
    $ 35.98万
  • 项目类别:
Core--Molecular biology
核心--分子生物学
  • 批准号:
    6254735
  • 财政年份:
    1999
  • 资助金额:
    $ 35.98万
  • 项目类别:
TRAINING PROGRAM IN MOLECULAR AND CELLULAR NEUROBIOLOGY
分子和细胞神经生物学培训计划
  • 批准号:
    2674708
  • 财政年份:
    1995
  • 资助金额:
    $ 35.98万
  • 项目类别:
TRAINING PROGRAM IN MOLECULAR AND CELLULAR NEUROBIOLOGY
分子和细胞神经生物学培训计划
  • 批准号:
    2890199
  • 财政年份:
    1995
  • 资助金额:
    $ 35.98万
  • 项目类别:

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