Neuronal Substrates of Learning in Apylsia

Apylsia 学习的神经元基质

• 批准号: 9514619
• 负责人: Gregory Clark
• 金额: $ 20万
• 依托单位: Princeton University
• 依托单位国家: 美国
• 项目类别: Standard Grant
• 财政年份: 1996
• 资助国家: 美国
• 起止时间: 1996-04-01 至 1999-03-31
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=9514619&HistoricalAwards=false
• 关键词: Neuronal; Substrates; Learning; Apylsia

9514619 Clark Learning and synaptic plasticity -- the modification of communication between nerve cells -- play a central role in a wide variety of cognitive and neuronal processes. Because a single neuron can make synaptic contacts with thousands of other neurons, a fundamental question is whether increases in synaptic strength are necessarily expressed cell-wide at all connections of a given neuron, or can instead be synapse- specific and so occur at only selected connections of the cell. To investigate synapse-specific facilitation, this research program utilizes a favorable simple model system, and focuses on cells known to exhibit learning-related increases in synaptic strength. Studies will first determine whether long-term ( 24 hr) as well-as short-term increases in synaptic strength can be synapse-specific. This is a critical issue, given that long-term facilitation appears to depend on changes in gene expression. The neurotransmitter serotonin will be applied selectively onto particular synapses in order to induce facilitation, and intracellular electrophysiological recordings will be used to test whether synaptic facilitation is greater at treated synapses compared with other synapses of the same cell. Second, studies will investigate underlying cellular mechanisms. These studies will provide new insights into the conceptual and mechanistic relationships between short-term and long- term memory, and illuminate key cellular and molecular steps underlying learning-related neuronal change.

学习和突触可塑性——神经细胞之间交流的改变——在各种认知和神经元过程中发挥着核心作用。因为单个神经元可以与数千个其他神经元进行突触接触，一个基本的问题是，突触强度的增加是否一定是在给定神经元的所有连接上表达的，还是可能是突触特异性的，因此只发生在细胞的选定连接上。为了研究突触特异性促进，本研究项目利用了一个有利的简单模型系统，并将重点放在已知表现出与学习相关的突触强度增加的细胞上。研究将首先确定突触强度的长期（24小时）和短期增加是否具有突触特异性。这是一个关键的问题，因为长期的促进似乎取决于基因表达的变化。神经递质5 -羟色胺将被选择性地应用于特定的突触以诱导易化，细胞内电生理记录将被用来测试与同一细胞的其他突触相比，治疗突触的突触易化是否更大。其次，研究将调查潜在的细胞机制。这些研究将为短期记忆和长期记忆之间的概念和机制关系提供新的见解，并阐明学习相关神经元变化的关键细胞和分子步骤。