Computational Models of Adaptive Neural Circuits

自适应神经电路的计算模型

基本信息

项目摘要

DESCRIPTION (provided by applicant): Two complementary approaches, one empirical and the other modeling, are being used to investigate the ways in which synaptic plasticity emerges from interactions among pre- and postsynaptic processes (e.g., presynaptic spike broadening, mobilization and depletion of transmitter, modulation of exocytosis, desensitization of postsynaptic receptors, and modulation of the numbers of transmitter receptors and transporters). The proposed studies will focus on the glutamatergic sensorimotor synapses that mediate withdrawal reflexes of Aplysia. Empirical studies, which are funded by NIH grant NS19895, characterize the biochemical and biophysical processes that underlie homo- and heterosynaptic plasticity. The modeling studies, which will be funding by the present proposal, will use these empirical data, and those in the published literature, to develop mathematical models of the synapse. The models will be manipulated to study the contributions of component processes to synaptic function and to identify critical parameters that warrant additional experimental examination. Particular attention will be focused on analyzing the responses of the synapse to brief bursts of presynaptic activity. Such bursts closely resemble the physiological responses of sensory neurons to test stimuli that are typically used in behavioral studies. Moreover, it has recently become clear that the traditional means of probing the synapse with a single presynaptic spike fails to reveal the full extent of modulatory processes that regulate synaptic efficacy. The proposed modeling studies will examine synaptic function and plasticity at multiple levels of organization, ranging from kinetic models of transmitter binding to receptors and transporters, to cellular models of synaptic transmission, to neural network models of presynaptic sensory neurons and a postsynaptic motor neuron. The specific aims of this project are: 1) Investigate the ways in which desensitization of glutamate (GLU) receptors and increases in the numbers of GLU transporters and receptors contribute to modulation of the PSP during brief bursts of presynaptic activity. 2) Investigate the relative contributions of pre- and postsynaptic processes to homo- and heterosynaptic modulation of the PSP during brief bursts of presynaptic activity. 3) Investigate the input-output relationship (i.e., the ability of presynaptic activity to drive the postsynaptic spiking) of the sensorimotor synapse during brief bursts of presynaptic activity.
描述(由申请人提供):两种互补方法,一种经验和另一种建模,用于研究突触可塑性从突触前和突触后过程之间的相互作用出现的方式(例如,突触前尖峰扩大,动员,动员,移动和转移器的耗竭,调节胞吐作用,突触后受体脱敏以及发射机受体和转运蛋白的数量的调节)。拟议的研究将重点放在谷氨酸能感觉运动突触,以介导垂直脂肪的戒断反射。由NIH Grant NS19895资助的实证研究表征了同性恋和异质性可塑性的生化和生物物理过程。建模研究将由本提案提供资金,将使用这些经验数据以及已发表的文献中的这些数据来开发突触的数学模型。这些模型将被操纵以研究组件过程对突触功能的贡献,并确定值得进行额外实验检查的关键参数。特别关注的是分析突触对短暂突触前活性突发的反应。这种爆发非常类似于感觉神经元在行为研究中通常使用的刺激的生理反应。此外,最近很明显,单个突触前尖峰探测突触的传统手段未能揭示调节突触功效的调节过程的全部范围。 所提出的建模研究将检查在多个组织下的突触功能和可塑性,从发射机与受体和转运蛋白的动力学模型到突触传播的细胞模型,再到突触前感觉神经元的神经网络模型,以及突触后运动神经元的神经网络模型。该项目的具体目的是:1)研究谷氨酸(GLU)受体脱敏的方式以及GLU转运蛋白和受体的数量增加在突触前活性的短暂突发中有助于PSP的调节。 2)研究突触前活性短暂爆发期间,突触前过程和突触后过程对PSP的同性突触调制的相对贡献。 3)研究在突触前活动的短暂突发中,研究了感觉运动突触的输入输出关系(即,突触前活动驱动突触后尖峰的能力)。

项目成果

期刊论文数量(10)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Current- and voltage-clamp recordings and computer simulations of Kenyon cells in the honeybee.
  • DOI:
    10.1152/jn.01259.2003
  • 发表时间:
    2004-06
  • 期刊:
  • 影响因子:
    2.5
  • 作者:
    D. Wüstenberg;Milena Boytcheva;B. Grünewald;J. Byrne;R. Menzel;D. A. Baxter
  • 通讯作者:
    D. Wüstenberg;Milena Boytcheva;B. Grünewald;J. Byrne;R. Menzel;D. A. Baxter
Teaching basic principles of neuroscience with computer simulations.
通过计算机模拟教授神经科学的基本原理。
Simulator for neural networks and action potentials.
Mechanisms underlying fictive feeding in aplysia: coupling between a large neuron with plateau potentials activity and a spiking neuron.
  • DOI:
    10.1152/jn.2002.87.5.2307
  • 发表时间:
    2002-05
  • 期刊:
  • 影响因子:
    2.5
  • 作者:
    Abraham J Susswein;I. Hurwitz;R. Thorne;J. Byrne;D. A. Baxter
  • 通讯作者:
    Abraham J Susswein;I. Hurwitz;R. Thorne;J. Byrne;D. A. Baxter
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Douglas Alan Baxter其他文献

Douglas Alan Baxter的其他文献

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{{ truncateString('Douglas Alan Baxter', 18)}}的其他基金

Computational Core Facility
计算核心设施
  • 批准号:
    6995176
  • 财政年份:
    2005
  • 资助金额:
    $ 21.75万
  • 项目类别:
Modeling plasticity in neurons and neural circuits
神经元和神经回路的可塑性建模
  • 批准号:
    6318433
  • 财政年份:
    2000
  • 资助金额:
    $ 21.75万
  • 项目类别:
Core--Computational facility
核心--计算设施
  • 批准号:
    6318435
  • 财政年份:
    2000
  • 资助金额:
    $ 21.75万
  • 项目类别:
Modeling plasticity in neurons and neural circuits
神经元和神经回路的可塑性建模
  • 批准号:
    6233342
  • 财政年份:
    1999
  • 资助金额:
    $ 21.75万
  • 项目类别:
Core--Computational facility
核心--计算设施
  • 批准号:
    6233360
  • 财政年份:
    1999
  • 资助金额:
    $ 21.75万
  • 项目类别:
COMPUTATIONAL MODELS OF ADAPTIVE NEURAL CIRCUITS
自适应神经电路的计算模型
  • 批准号:
    6188709
  • 财政年份:
    1995
  • 资助金额:
    $ 21.75万
  • 项目类别:
COMPUTATIONAL MODELS OF ADAPTIVE NEURAL CIRCUITS
自适应神经电路的计算模型
  • 批准号:
    6394653
  • 财政年份:
    1995
  • 资助金额:
    $ 21.75万
  • 项目类别:
Computational Models of Adaptive Neural Circuits
自适应神经电路的计算模型
  • 批准号:
    6775224
  • 财政年份:
    1995
  • 资助金额:
    $ 21.75万
  • 项目类别:
COMPUTATIONAL MODELS OF ADAPTIVE NEURAL CIRCUITS
自适应神经电路的计算模型
  • 批准号:
    2850674
  • 财政年份:
    1995
  • 资助金额:
    $ 21.75万
  • 项目类别:
COMPUTATIONAL MODELS OF ADAPTIVE NEURAL CIRCUITS
自适应神经电路的计算模型
  • 批准号:
    2460737
  • 财政年份:
    1995
  • 资助金额:
    $ 21.75万
  • 项目类别:

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Modeling the dynamics of genes and excitable membranes
模拟基因和可兴奋膜的动力学
  • 批准号:
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  • 财政年份:
    2000
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  • 项目类别:
Modeling plasticity in neurons and neural circuits
神经元和神经回路的可塑性建模
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  • 批准号:
    6233340
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Modeling plasticity in neurons and neural circuits
神经元和神经回路的可塑性建模
  • 批准号:
    6233342
  • 财政年份:
    1999
  • 资助金额:
    $ 21.75万
  • 项目类别:
Computational Models of Adaptive Neural Circuits
自适应神经电路的计算模型
  • 批准号:
    6775224
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