Postsynaptic Cellular Mechanisms of Learning in Aplysia

描述（由申请人提供）：该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，本项目将试图确定是否突触后神经调节机制引起的尾神经休克在经典条件反射相互作用，以任何方式与经典条件反射的活动依赖性关联组件。在行为可塑性下的神经元回路的Aesthesia虹吸撤回反射是明确的和相对简单的。此外，存在于失智症的感觉运动突触处的细胞机制与海马中的CA 3-CA 1突触具有许多相同的特性。这两种突触都具有NMDA依赖的LTP，并受到神经调质的影响，但哺乳动物系统的复杂性阻碍了将突触变化与动物所表现出的实际学习联系起来。失智症中经典条件反射的神经回路定义明确且相对简单，因此突触变化更容易归因于动物的行为可塑性。这些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了解人类记忆疾病，如阿尔茨海默氏症和其他相关的痴呆症。

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.