CELLULAR MECHANISMS OF LEARNING IN APLYSIA

海兔学习的细胞机制

• 批准号: 3385110
• 负责人: MARC KLEIN
• 金额: $ 9.71万
• 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/3385110
• 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; 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.

致敏和经典条件是两种学习形式， 在整个整个过程中分别发生了非缔合和联想 动物王国，包括人。在海洋软体动物中，两者都 致敏和经典条件涉及增加 发射器释放，称为异突触促进，从 机械感受器感官神经元的介导防御性的途径 提取行为。 伴随着许多细胞现象，其中包括 钾电流减少，峰值持续时间增加 数量，以及钙处理的改变。较早的工作 表明促进涉及动员生化级联 这导致细胞内循环腺苷单磷酸盐的增加 （CAMP）以及随之而来的神经元底物的磷酸化 cAMP依赖性蛋白激酶。 拟议的项目具有三倍的目标：1。重新检查 促进营地。这个问题是由初步提示的 表明仅营地增加的实验可能是 不足以说明促进。 2。确定哪个 与促进作用相关的细胞现象是因果 不是，并确定可以考虑多少便利化 每个过程。 3。检查与 促进的依赖于活动的放大，以确定是否是 已提出，经典条件仅涉及 敏感性的过程或新机制是 涉及。 这些问题将通过检查1）对 用新的代理促进治疗感觉神经元 那会影响阵营的级联； 2）时间课程和效果 在不同的操作中，每个促进相关 与促进本身的现象相比，现象; 3）细胞 促进的活动依赖性扩增的相关性，a 经典条件的基础机制。