CELLULAR MECHANISMS OF LEARNING IN APLYSIA

海兔学习的细胞机制

• 批准号: 3385108
• 负责人: MARC KLEIN
• 金额: $ 8.69万
• 依托单位: CLINICAL RESEARCH INSTITUTE OF MONTREAL
• 依托单位国家: 美国
• 财政年份: 1989
• 资助国家: 美国
• 起止时间: 1989-09-30 至 1992-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3385108
• 关键词: Gastropoda; action potentials; association learning; calcium flux; conditioning; cyclic AMP; electrophysiology; mechanoreceptors; membrane potentials; microelectrodes; molecular psychobiology; neurobiology; neurotransmitters; receptor sensitivity; sensory mechanism; single cell analysis; voltage /patch clamp

Sensitization and classical conditioning are two forms of learning, respectively non-associative and associative, that occur throughout the animal kingdom, including in man. In the marine mollusc Aplysia, both sensitization and classical conditioning involve increases in transmitter release, called heterosynaptic facilitation, from mechanoreceptor sensory neurons of the pathways that mediate defensive withdrawal behaviors. A number of cellular phenomena accompany this facilitation, among them a reduction in potassium current, an increase in spike duration and number, and an alteration in the handling of calcium. Earlier work showed that facilitation involves mobilization of a biochemical cascade that results in a rise in intracellular cyclic adenosine monophosphate (cAMP) and the consequent phosphorylation of neuronal substrates by cAMP-dependent protein kinase. The proposed project has a threefold aim: 1. To re-examine the role of CAMP in facilitation. This question is prompted by preliminary experiments that suggest that an increase in cAMP alone may be insufficient to account for facilitation. 2. To determine which of the cellular phenomena associated with facilitation are causal and which are not, and to determine how much of the facilitation can be accounted for by each process. 3. To examine the cellular phenomena associated with activitydependent amplification of facilitation to determine whether, as has been proposed, classical conditioning involves only enhancement of processes that underlie sensitization, or whether new mechanisms are involved. These questions will be addressed by examining 1) the effects on facilitation of treating sensory neurons with newly-available agents that influence the CAMP cascade; 2) the time courses of, and the effects of different manipulations on, each of the facilitation-associated phenomenal compared to those of the facilitation itself; and 3) cellular correlates of activity-dependent amplification of facilitation, a mechanism underlying classical conditioning.

敏化和经典条件反射是学习的两种形式， 分别是非关联和关联，它们发生在整个过程中 动物王国，包括人类。在海洋软体动物海兔中，两者 敏化和经典条件反射涉及增加 递质释放，称为异质突触促进， 介导防御通路的机械感受器感觉神经元 戒断行为。 许多细胞现象伴随着这种促进作用，其中包括 钾电流减少，尖峰持续时间增加和 数量，以及钙处理的改变。早期工作 表明促进涉及生化级联的动员 导致细胞内环磷酸腺苷增加 (cAMP) 以及随后的神经元底物磷酸化 cAMP 依赖性蛋白激酶。 拟议项目有三个目标： 1. 重新审视 CAMP 促进。这个问题是由初步提出的 实验表明，单独增加 cAMP 可能 不足以解释便利化。 2. 确定哪一个 与促进相关的细胞现象是因果关系，并且是 不，并确定可以解释多少便利 通过每个过程。 3. 检查与以下相关的细胞现象 促进的活动依赖性放大，以确定是否，如 已经提出，经典条件反射只涉及增强 致敏的过程，或者是否有新的机制 涉及。 这些问题将通过检查 1) 对 促进用新药治疗感觉神经元 影响 CAMP 级联； 2）时间进程和效果 不同的操作，每个与便利相关的 与便利本身相比是惊人的； 3) 蜂窝 活动依赖性促进放大的相关性，a 经典条件反射的机制。