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ASSOCIATIVE INFORMATION PROCESSING CELLULAR MECHANISMS

ASSOCIATIVE INFORMATION PROCESSING CELLULAR MECHANISMS
关联信息处理细胞机制
批准号:
3376840
负责人:
EDGAR T. WALTERS
金额:
$13.57万
依托单位国家:
美国
项目类别:
财政年份:
1987
资助国家:
美国
项目状态:
已结题
起止时间:
1987-02-01 至 1996-01-31

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中文摘要
翻译
长期的目标是分析细胞的机制, 神经系统的两个重要功能:(1) 将给定的刺激与新的运动反应(刺激-反应)相关联 或S-R学习),以及(2)长期感觉可改变性。 这一目标 需要发展的准备工作,涉及明确的行为 改变和识别的神经网络,允许直接分析 生理机制。 在初步研究基础上, 海洋腹足类的虹吸管、尾部、头部和副足,Aaprissia,完整 和半完整的准备工作将被开发,显示收购 在将足旁刺激与头部配对后的新虹吸反应或 尾部刺激 这种S-R条件反射的电生理学相关性 将在鉴定的虹吸运动神经元和中间神经元中进行检查。 两 新的S-R连接的发展假设将被测试 使用细胞内记录、电压钳和量子分析 技术. 长期感觉记忆将在中央研究 以及足旁感觉神经元的外周突起,它们提供特殊的 感官分析的优势。 一般的假设是, 感觉系统中的信息存储利用了进化的机制, 将测试损伤后的感觉补偿。 A的贡献 特定细胞关联机制-活性依赖性外在 将测试ADEM对感觉的可修饰性。 几 潜在的ADEM相关的信号有效性增强, 联想条件反射和感受野的损伤将 检查:突触易化,中枢和/或外周增加 兴奋性和外周和/或中枢突起的发芽。 这些 研究应提供关于一般学习机制的基本信息, 感觉补偿和神经元再生 有助于了解正常和异常的生理 人类神经系统的可塑性。
英文摘要
The long-term objective is to analyze the cellular mechanisms underlying two important capabilities of the nervous system: (1) the ability to associate a given stimulus with a novel motor response (stimulus-response or S-R learning), and (2) long-term sensory modifiability. This objective requires the development of preparations, involving well-defined behavioral alterations and identified neuronal networks, that permit direct analysis of physiological mechanisms. Building on preliminary studies using the siphon, tail, head, and parapodia of the marine gastropod, Aplysia, intact and semi-intact preparations will be developed that show the acquisition of novel siphon responses after pairing parapodial stimulation with head or tail stimulation. Electrophysiological correlates of this S-R conditioning will be examined in identified siphon motor neurons and interneurons. Two hypotheses for the development of novel S-R connections will be tested using intracellular recording, voltage clamp, and quantal analysis techniques. Long-term sensory memory will be investigated in the central and peripheral processes of parapodial sensory neurons, which offer special advantages for sensory analysis. The general hypothesis that associative information storage in sensory systems makes use of mechanisms evolved for sensory compensation after injury will be tested. The contribution of a specific cellular associative mechanism - activity-dependent extrinsic modulation (ADEM) - to sensory modifiability will be tested. Several potential ADEM-related enhancements of signaling effectiveness produced by associative conditioning and by injury of the receptive field will be examined: synaptic facilitation, increased central and/or peripheral excitability, and sprouting of peripheral and/or central processes. These studies should provide basic information on general mechanisms of learning, sensory compensation, and neuronal regeneration that may eventually contribute to an understanding of normal and abnormal physiological plasticity within the human nervous system.
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