ANALYSIS OF THE NEURAL CONTROL OF BEHAVIOR

行为的神经控制分析

基本信息

批准号：
3400004
负责人：
John H Byrne
金额：
$ 12.65万
依托单位：
UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
依托单位国家：
美国
项目类别：
财政年份：
1983
资助国家：
美国
起止时间：
1983-04-01 至 1993-03-31
项目状态：
已结题

项目摘要

A classical conditioning protocol applied directly to individual tail sensory neurons in Aplysia results in an associative modification of the monosynaptic connections to tail motor neurons. Sensory neurons receiving a conditioned stimulus (CS, intracellular activation of the sensory neuron) immediately before the unconditioned stimulus (US, tail shock) show significantly more synaptic facilitation than sensory neurons exposed to the US alone or to unpaired CS and US applications. An analog of the classical conditioning paradigm produces a selective amplification of the cAMP content of isolated sensory neuron clusters. These results indicate that a pairing-specific enhancement of cAMP levels may be a biochemical mechanism for associative learning. Experiments proposed here are designed to extend these analyses. Specifically, we will examine 1) whether Ca2+ serves as the signal for the induction of the associative change, 2) whether cAMP levels in the sensory neurons are increased during simple forms of learning such as sensitization and classical conditioning, 3) the contribution of spike broadening in the sensory neurons to synaptic facilitation and behavioral modifications, 4) the properties of the neural circuit elements mediating the tail withdrawal reflex and effects of the US, and 5) the coordination of synergistic defensive responses triggered by tail stimulation. The tail withdrawal reflex offers a unique opportunity to investigate the cellular and molecular basis of learning. Few systems offer all the advantages found in this preparation; a simple stereotyped behavior for which the neural circuitry is relatively well defined, a large homogeneous population of identifiable cells that are accessible for biochemical and biophysical assay, and a testable hypothesis. Continued analysis of this system promises to yield much additional information concerning the cellular mechanisms underlying associative and nonassociative learning.

直接应用于个体尾部的经典调理方案海兔的感觉神经元导致了与尾部运动神经元的单突触连接。感觉神经元接收条件刺激（CS，感觉神经元的细胞内激活）无条件刺激（美国，尾部冲击）即将出现之前与接触的感觉神经元相比，突触促进明显更多单独的美国或未配对的 CS 和美国应用程序。一个类似的经典条件作用范式产生选择性放大孤立的感觉神经元簇的 cAMP 含量。这些结果表明 cAMP 水平的配对特异性增强可能是一种生化作用联想学习机制。这里提出的实验是设计的来扩展这些分析。具体来说，我们将检查 1) 是否 Ca2+ 作为诱导联想变化的信号，2) 感觉神经元中的 cAMP 水平是否在简单过程中增加学习形式，例如敏化和经典条件反射，3）感觉神经元尖峰增宽对突触的贡献促进和行为改变，4）神经元的特性介导尾部撤回反射的电路元件及其影响美国，以及5）协调协同防御反应尾部刺激。尾部撤退反射提供了一个独特的机会来研究学习的细胞和分子基础。很少有系统能够提供所有该制剂的优点；一个简单的刻板行为其中神经回路定义相对明确，是一个大的同质可识别的细胞群，可用于生化和生物物理测定和可检验的假设。继续分析这个系统有望提供更多有关联想和非联想学习背后的细胞机制。