CELLULAR ANALYSIS OF LEARNING

学习的细胞分析

基本信息

批准号：
3411749
负责人：
JOSEPH FARLEY
金额：
$ 10.81万
依托单位：
TRUSTEES OF INDIANA UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
1989
资助国家：
美国
起止时间：
1989-01-01 至 1991-12-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/3411749
关键词：
Gastropoda association learning biophysics calmodulin conditioning electrophysiology interneurons membrane permeability neural information processing phosphorylation photobiology potassium channel protein kinase C serotonin stimulus /response synapses visual photoreceptor

项目摘要

Pairings of light and rotation result in a long-term suppression of phototaxic behavior for the mollusc Hermissenda. Two K+ currents in Hermissenda Type B photoreceptors (IA and IK-Ca) are reduced, and a calcium current (ICa) is enhanced, by associative training. Type A photoreceptor light responses are also changed and increases in a K current (IK-Ca) may be responsible. These long-lasting changes in ionic conductances comprise a biophysical basis for long-term information storage. We propose to study the cellular mechanisms by which these long term ionic current changes occur, and in particular the roles that serotonin (5-HT) and protein kinase C (PKC)-activation may play. We will condition the isolated nervous system of Hermissenda using a protocol which preserves the normal synaptic input to Type B cells (intact synapses protocol). Current-clamp and two-electrode voltage clamp techniques will be used to determine the ionic basis of short-term training-produced changes in Type B cells: cumulative depolarization and decreased membrane conductance. The role of PKC-dependent and calcium/calmodulin-dependent phosphorylation pathways in these changes will be assessed. We shall study the gating, permeation, pharmacology, and possible phosphorylational control of K+ channels from Hermissenda Type B cells through, single channel measurements of ion fluxes, and will determine the ability of protein kinase C to modify K+ channel properties.

光和旋转的配对会导致长期抑制软体动物 Hermissenda 的趋光行为。两K+ Hermissenda B 型光感受器（IA 和 IK-Ca）中的电流为通过缔合，钙电流（ICa）减少，钙电流（ICa）增强训练。 A型光感受器的光反应也发生了变化 K 电流 (IK-Ca) 的增加可能是原因。这些离子电导的持久变化包括生物物理为长期信息存储奠定基础。我们建议研究这些长的细胞机制术语离子电流发生变化，特别是作用血清素 (5-HT) 和蛋白激酶 C (PKC) 激活可能发挥作用。我们将使用以下方法调节 Hermissenda 的孤立神经系统保留 B 型正常突触输入的协议细胞（完整突触协议）。电流钳和两电极电压钳技术将用于确定离子基础短期训练引起的 B 型细胞变化：累积去极化和膜电导降低。这 PKC 依赖性和钙/钙调蛋白依赖性的作用将评估这些变化中的磷酸化途径。我们将研究门控、渗透、药理学以及可能的 Hermissenda B 型 K+ 通道的磷酸化控制细胞通过离子通量的单通道测量，并将确定蛋白激酶 C 修饰 K+ 通道的能力特性。