CELLULAR ANALYSIS OF LEARNING

光线和旋转的组合导致了长期的抑制 软体动物赫米森达的趋光行为。两千 HermissendaB型光感受器(IA和Ik-Ca)的电流是 降低，钙电流(ICA)增强，通过联合 训练。A型光感受器的光反应也发生了变化 K电流(Ik-Ca)的增加可能与此有关。这些 离子电导的长期变化包括生物物理 为信息的长期存储奠定了基础。 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-羟色胺)和蛋白激酶C(PKC)的激活可能起作用。 我们将用来调节赫米森达的孤立神经系统 保留B型的正常突触输入的方案 细胞(完整突触协议)。电流钳和双电极 将使用电压钳位技术来确定离子基础 短期训练导致的B细胞变化的可能性： 累积去极化和膜电导下降。这个 蛋白激酶C依赖和钙/钙调蛋白依赖的作用 这些变化中的磷酸化途径将被评估。 我们将研究门控、渗透、药理和可能的 HermissendaB型钾离子通道的磷酸化调控 电池通过，离子通量的单通道测量，并将 测定蛋白激酶C对钾通道的修饰能力 属性。

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.