CHANGES OF CAMKII INDUCED WITH LTP AND LTD

LTP 和 LTD 引起的 CAMKII 变化

• 批准号: 2647498
• 负责人: YANNAN OUYANG
• 金额: $ 3.02万
• 依托单位: CALIFORNIA INSTITUTE OF TECHNOLOGY
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-08-01 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/2647498
• 关键词: animal genetic material tag; antisense nucleic acid; calmodulin dependent protein kinase; confocal scanning microscopy; dendritic cells; enzyme activity; hippocampus; isozymes; laboratory mouse; long term potentiation; neural plasticity; oligonucleotides; phosphoproteins; phosphorylation; tissue /cell culture

DESCRIPTION The proposed experiments focus on visualization of an quantitation of the changes in autophosphorylated and non-phosphorylated Calcium/calmodulin dependent protein kinase II (CaMKII) in hippocampal slices after induction of LTP or LTD. Induction of new synthesis of CaMKII by stimulation that induce LTP will be verified with inhibitors of protein synthesis, with phosphorothioate antisense oligonucleotide, or with adenovirus delivered antisense RNA. A better understanding of the role of CaMKII in synaptic plasticity and of possible "metaplasticity" mechanism is expected. Such an understanding may lead to clues to improve learning and memory in people with diseases such as Alzheimer's disease.

描述 拟议的实验侧重于可视化的量化 自磷酸化和非磷酸化钙/钙调蛋白的变化 诱导后大鼠海马脑片中依赖蛋白激酶II的表达 LTP或Ltd.通过刺激诱导CaMKII的新合成 诱导LTP将通过蛋白质合成的抑制剂进行验证， 硫代反义寡核苷酸或腺病毒载体 反义RNA。更好地理解CaMKII在突触中的作用 可塑性和可能的“变塑性”机制是可望的。这样的一种 理解可能会带来改善人们学习和记忆的线索 患有阿尔茨海默氏症等疾病。