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Spatial and temporal aspects of synaptic plasticity.

机译:突触可塑性的时空方面。

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摘要

The notion that changes in synaptic efficacy underlie learning and memory processes is now widely accepted even if definitive proof of the synaptic plasticity and memory hypothesis is still lacking. When learning occurs, patterns of neural activity representing the occurrence of events cause changes in the strength of synaptic connections within the brain. Reactivation of these altered connections constitutes the experience of memory for these events and for other events with which they may be associated. These statements summarize a long-standing theory of memory formation that we refer to as the synaptic plasticity and memory hypothesis. Since activity-dependent synaptic plasticity is induced at appropriate synapses during memory formation, and is both necessary and sufficient for the information storage, we can speculate that a methodological study of the synapse will help us understand the mechanism of learning. Random events underlie a wide range of biological processes as diverse as genetic drift and molecular diffusion, regulation of gene expression and neural network function. Additionally spatial variability may be important especially in systems with nonlinear behavior. Since synapse is a complex biological system we expect that stochasticity as well as spatial gradients of different enzymes may be significant for induction of plasticity.;In that study we address the question "how important spatial and temporal aspects of synaptic plasticity may be". We developed methods to justify our basic assumptions and examined the main sources of variability of calcium dynamics. Among them, a physiological method to estimate the number of postsynaptic receptors as well as a hybrid algorithm for simulating postsynaptic calcium dynamics. Additionally we studied how synaptic geometry may enhance any possible spatial gradient of calcium dynamics and how that spatial variability affect plasticity curves. Finally, we explored the potential of structural synaptic plasticity to provide a metaplasticity mechanism specific for the synapse.
机译:即使仍然缺乏关于突触可塑性和记忆假说的确切证据,关于突触功效变化是学习和记忆过程的基础的观点现已被广泛接受。当学习发生时,代表事件发生的神经活动模式会引起大脑内突触连接强度的变化。重新激活这些更改的连接构成了这些事件以及可能与之关联的其他事件的记忆体验。这些陈述总结了长期存在的记忆形成理论,我们称其为突触可塑性和记忆假设。由于依赖活动的突触可塑性在记忆形成过程中在适当的突触中被诱导,并且对于信息存储既必要又足够,因此我们可以推测,对突触进行的方法学研究将有助于我们了解学习的机制。随机事件是广泛的生物学过程的基础,例如遗传漂移和分子扩散,基因表达调控和神经网络功能。另外,空间可变性可能很重要,尤其是在具有非线性行为的系统中。由于突触是一个复杂的生物系统,我们期望随机性以及不同酶的空间梯度对于诱导可塑性具有重要意义。在该研究中,我们解决了“突触可塑性的时空方面可能有多重要”的问题。我们开发了证明基本假设合理性的方法,并研究了钙动力学变化的主要来源。其中,一种用于估计突触后受体数量的生理方法,以及一种用于模拟突触后钙动力学的混合算法。此外,我们研究了突触几何形状如何增强钙动力学的任何可能的空间梯度,以及该空间变异性如何影响可塑性曲线。最后,我们探讨了结构突触可塑性为突触提供特异的可塑性机制的潜力。

著录项

  • 作者

    Kalantzis, Georgios.;

  • 作者单位

    The University of Texas Graduate School of Biomedical Sciences at Houston.;

  • 授予单位 The University of Texas Graduate School of Biomedical Sciences at Houston.;
  • 学科 Biology Neuroscience.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 131 p.
  • 总页数 131
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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