CELLULAR ANALYSIS OF LEARNING

成对的光和旋转导致了长期的抑制 的趋光性行为。 两个K+ Hermissenda B型光感受器（IA和IK-Ca）中的电流是 降低，钙电流（伊卡）增强，通过联合 训练 A型感光细胞的光反应也发生了变化 并且K电流（IK-Ca）的增加可能是原因。 这些 离子电导的长期变化包括生物物理学的 长期信息存储的基础。 我们建议研究这些长时间的细胞机制， 术语离子电流发生变化，特别是 5-羟色胺（5-HT）和蛋白激酶C（PKC）激活可能起作用。 我们将使用 保留正常突触输入到类型B的协议 细胞（完整突触方案）。 电流钳双电极 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： 累积去极化和降低的膜电导。 的 PKC依赖性和钙/钙调素依赖性的作用 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，和可能的 Hermissenda B型钾通道的磷酸化调控 细胞通过，离子通量的单通道测量，并将 测定蛋白激酶C修饰K+通道的能力 特性.

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.