CHANGES OF CAMKII INDUCED WITH LTP AND LTD

LTP 和 LTD 引起的 CAMKII 变化

• 批准号: 2883599
• 负责人: YANNAN OUYANG
• 金额: $ 3.84万
• 依托单位: CALIFORNIA INSTITUTE OF TECHNOLOGY
• 依托单位国家: 美国
• 财政年份: 1999
• 资助国家: 美国
• 起止时间: 1999-03-01 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/2883599
• 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 所提出的实验集中在可视化的定量的 自磷酸化和非磷酸化钙/钙调蛋白的变化 诱导后海马脑片中依赖性蛋白激酶II（CaMK II） LTP或LTD的刺激诱导CaMK II的新合成， 诱导LTP将用蛋白质合成抑制剂进行验证， 硫代磷酸反义寡核苷酸，或用腺病毒递送 反义RNA更好地理解CaMK Ⅱ在突触中的作用 塑性和可能的“亚塑性”机制。这样的 理解可能会为改善人们的学习和记忆提供线索 老年痴呆症之类的疾病。