Structural Changes of Synaptic Plasticity in Aplysia

海兔突触可塑性的结构变化

• 批准号: 6639787
• 负责人: DANIEL J GOLDBERG
• 金额: $ 29.84万
• 依托单位: COLUMBIA UNIVERSITY HEALTH SCIENCES
• 依托单位国家: 美国
• 财政年份: 2001
• 资助国家: 美国
• 起止时间: 2001-04-15 至 2006-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6639787
• 关键词: Aplysia; actins; afferent nerve; cell adhesion molecules; cytochalasins; enzyme activity; fluorescence microscopy; learning; myosin light chain kinase; neural plasticity; neuropharmacology; protein kinase A; synapses

DESCRIPTION: Structural changes accompany, and are assumed to be important for, certain types of long-term synaptic plasticity. The synapse of the mechanosensory neuron (SN) on the gill motor neuron (L7) in the central nervous system of Aplysia has been one of the most productive preparations for studying long-term synaptic plasticity. Large changes in the number of synaptic varicosities and the size of the axonal arbor accompany both facilitation and inhibition of this synapse. New methodological capabilities allowing high resolution imaging of the cells will be used to examine how structural changes occur at the cellular and molecular levels and how they contribute to the expression of plasticity. Recent data point to the importance for structural change of rapid changes in actin dynamics at presynaptic varicosities. The molecular underpinnings of these changes will be examined. Along with this rapid, local change at the terminal, protein synthesis induced in the cell body of the presynaptic neuron by the plasticizing stimulus is required for the growth of presynaptic varicosities and axonal arbor. Which aspects of this growth depend on this protein synthesis will be assessed. New presynaptic varicosities must persist days or more to contribute to long-term facilitation. Experiments will examine the hypothesis that levels at the new varicosities of the adhesion molecule apCAM are involved in maintaining the varicosities. Lastly, the contribution of structural changes to the maintained expression of long-term facilitation will be assessed by blocking those changes. Synaptic plasticity is likely a cellular mechanism for learning, with long-term plasticity underlying memory. By contributing to a cellular and molecular understanding of learning and memory, findings from this project might contribute to the design of therapeutic approaches for disorders of cognitive function, like Alzheimer's disease.

描述： 结构性变化伴随着某些变化，并且被认为对某些变化很重要 长期突触可塑性的类型。机械感觉突触 中枢神经系统鳃运动神经元（L7）上的神经元（SN） 海兔是长期研究最有效的准备之一 突触可塑性。突触静脉曲张数量的巨大变化 轴突乔木的大小伴随着这种作用的促进和抑制 突触。新的方法能力允许高分辨率成像 这些细胞将用于检查细胞结构如何发生变化 和分子水平以及它们如何促进可塑性的表达。 最近的数据表明，经济快速变化对结构性变革的重要性 突触前静脉曲张的肌动蛋白动力学。的分子基础 将审查这些变化。随着这种快速的局部变化 突触前神经元细胞体中诱导的末端蛋白质合成 突触前生长需要塑化刺激 静脉曲张和轴突乔木。这种增长取决于哪些方面 将评估蛋白质合成。新的突触前静脉曲张必须持续存在 天或更长时间，以促进长期便利。实验将检验 粘附分子新的静脉曲张水平的假设 apCAM 参与维持静脉曲张。最后，贡献 长期促进作用的维持表达的结构性变化将 通过阻止这些更改来进行评估。突触可塑性可能是一种细胞 学习机制，记忆具有长期可塑性。经过 有助于细胞和分子对学习和记忆的理解， 该项目的发现可能有助于治疗方案的设计 治疗认知功能障碍（如阿尔茨海默病）的方法。