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Memory following CaMKII Loss in Hippocampal Subregions

Memory following CaMKII Loss in Hippocampal Subregions
海马分区 CaMKII 丢失后的记忆
批准号：
6815813
负责人：
Brian J Wiltgen
金额：
$4.4万
依托单位：
UNIVERSITY OF CALIFORNIA LOS ANGELES
依托单位国家：
美国
项目类别：
财政年份：
2004
资助国家：
美国
项目状态：
已结题
起止时间：
2004-01-01 至 2006-12-31
来源：
https://reporter.nih.gov/project-details/6815813
关键词：
behavior testbiological modelscalmodulin dependent protein kinaseconditioningdentate gyruselectrophysiologyenzyme activitygene deletion mutationgene targetinghippocampuslearninglong term potentiationmemorymolecular biologymolecular psychobiologyneural plasticityneurochemistrypostdoctoral investigatorprotein structure functionpsychobiologytissue /cell culturetransfection /expression vector

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英文摘要
DESCRIPTION (provided by applicant): These studies are designed to determine the role of alpha-CaMKII in memory formation. Specifically, the effects of alpha-CaMKII deletion in distinct hippocampus subregions (CA1, dentate gyrus) will be examined. Deletion of alpha-CAMKII will be accomplished using contemporary knockout technology and targeted viral-vector infusions. Electrophysiological analyses will determine the effects of alpha-CaMKII deletion on long-term potentiation (LTP), a cellular model of learning and memory. Behavioral analyses will examine the effects of alpha-CaMKII loss on specific mnemonic functions mediated by each hippocampus subregion. The ultimate goal of these studies is to further our understanding of the molecular mechanisms that underlie memory formation in humans. Hippocampal dysfunction caused by disease (e.g., Alzheimer's, Korsakoff's), aging or damage produces severe memory loss. Understanding the molecular mechanisms that underlie hippocampus-dependent memory formation should provide insight into disorders caused by the dysfunction of this brain region.
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