Postsynaptic Cellular Mechanisms of Learning in Aplysia

海兔的突触后细胞学习机制

• 批准号: 6585209
• 负责人: Adam Christopher Roberts
• 金额: $ 2.51万
• 依托单位: UNIVERSITY OF CALIFORNIA LOS ANGELES
• 依托单位国家: 美国
• 财政年份: 2003
• 资助国家: 美国
• 起止时间: 2003-07-01 至 2005-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6585209
• 关键词: Aplysia; NMDA receptors; behavioral habituation /sensitization; calcium flux; conditioning; exocytosis; hippocampus; learning; long term potentiation; memory; motor neurons; neuropsychology; neuroregulation; predoctoral investigator; sensorimotor system; synapses

DESCRIPTION (provided by applicant): The central objective of this project is to elucidate the neuronal mechanisms of classical conditioning and sensitization. Furthermore, this project will seek to ascertain if postsynaptic neuromodulatory mechanisms elicited by tail nerve shock during classical conditioning interacts in any way with the activity-dependent associative component of classical conditioning. The neuronal circuitry underlying the behavioral plasticity of the Aplysia siphon withdrawal reflex is well defined and relatively simple. Also, the cellular mechanisms present at the sensorimotor synapse of the Aplysia share many of the same properties of CA3-CA1 synapses in the hippocampus. Both synapses have NMDA-dependent LTP and are influenced by neuromodulators, but the complexity of the mammalian system hinders connecting synaptic changes to the actual learning exhibited by the animal. The neural circuitry underlying classical conditioning in Aplysia is well defined and relatively simplistic, therefore synaptic changes are more readily attributed to the behavioral plasticity of the animal. The proposed experiments will increase our knowledge of synaptic plasticity and provide a basis for understanding the synaptic processes underlying human learning and memory. The increased knowledge may contribute to the understanding of human-memory diseases such as Alzheimer's and other related dementias.

描述（由申请人提供）：本项目的中心目标是阐明经典条件反射和敏化的神经元机制。此外，本项目将试图确定经典条件反射过程中尾神经休克引发的突触后神经调节机制是否以任何方式与经典条件反射的活动依赖性联想成分相互作用。虹吸退缩反射行为可塑性的神经回路是明确的，相对简单。此外，海马感觉运动突触的细胞机制与海马的CA3-CA1突触具有许多相同的特性。这两种突触都具有依赖于nmda的LTP，并受到神经调节剂的影响，但哺乳动物系统的复杂性阻碍了将突触变化与动物表现出的实际学习联系起来。海兔经典条件反射的神经回路定义明确，相对简单，因此突触变化更容易归因于动物的行为可塑性。提出的实验将增加我们对突触可塑性的认识，并为理解人类学习和记忆的突触过程提供基础。增加的知识可能有助于理解人类记忆疾病，如阿尔茨海默氏症和其他相关的痴呆症。