CELLULAR MECHANISMS AND FUNCTIONAL CONTRIBUTION BI-DIRECTIONAL SYNAPTIC PLASTICI

细胞机制和功能贡献双向突触塑料

• 批准号: 7720350
• 负责人: Brian Donald Burrell
• 金额: $ 19万
• 依托单位: UNIVERSITY OF SOUTH DAKOTA
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-06-01 至 2009-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7720350
• 关键词: Action Potentials; Adaptive Behaviors; Affect; Amygdaloid structure; Behavioral; Biological Models; Cell physiology; Cells; Chromosome Pairing; Computer Retrieval of Information on Scientific Projects Database; Funding; Grant; Hippocampus (Brain); Institution; Interneurons; Learning; Leeches; Long-Term Depression; Long-Term Potentiation; Mediating; Memory; N-Methyl-D-Aspartate Receptors; Neuronal Plasticity; Neurons; Numbers; Output; Pattern; Play; Reflex action; Research; Research Personnel; Resources; Role; Skin; Source; Specificity; Stimulus; Synapses; Synaptic Transmission; Synaptic plasticity; T-Lymphocyte; Thinking; Touch sensation; United States National Institutes of Health; Visual Cortex; base; classical conditioning; improved; neuromechanism; postsynaptic; research study; response

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Learning is perhaps the most malleable form of adaptive behavior and activity-dependent changes in synaptic transmission, such as long-term potentiation (LTP) or long-term depression (LTD), are thought to play a critical role in learning and subsequent memory formation. An emerging issue in the study of activity-dependent synaptic plasticity and its contribution to learning has been the realization that changes initiated at one synapse can spread to other inactive synapses. The induction of LTP at one set of synapses that simultaneously leads to LTD in surrounding inputs to a shared postsynaptic neuron is one example that has been observed in synapses in the hippocampus, visual cortex and amygdala. How this homosynaptic LTP and heterosynaptic LTD are generated, how they interact and their functional relevance is crucial to understanding the cellular basis of learning in particular and adaptive behavior in general. In the leech CNS, induction of LTP in synaptic connections between touch mechanoreceptive neurons (T-cells) and the S-cell (an interneuron known to be critical for some forms of learning of the defensive shortening reflex) also produces LTD in synapses made by non-tetanized T-cells onto the same postsynaptic S-cell. Homosynaptic LTP (homLTP) at T-S synapses is NMDA receptor independent while heterosynaptic LTD is NMDA receptor dependent (Burrell & Sahley, 2004). One possible function of this pattern of plasticity is to "tune" afferent input to a postsynaptic cell leading to improved stimulus specificity. Using the leech model system we propose to examine the cellular mechanisms that mediate homLTP and hetLTD. Furthermore, we will examine how induction of homLTP/hetLTD affects the functional output (in terms of number of action potentials) of the S-cell in response to touch cell input initiated at the skin. Finally, we will determine whether homLTP/hetLTD contributes to stimulus specificity between learned and neutral stimuli during associative learning of the shortening reflex. This project adheres to the Center?s theme of Neural Mechanisms of Adaptive Behavior in that the proposed experiments span from studies of cellular processes mediating neuroplasticity to the effects of such plasticity on learning at the behavioral level.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 学习可能是适应行为中最具可塑性的形式，突触传递中的活动依赖性变化，例如长时程增强（LTP）或长时程抑制（LTD），被认为在学习和随后的记忆形成中发挥着关键作用。 在活动依赖性突触可塑性及其对学习的贡献的研究中，一个新出现的问题是，在一个突触开始的变化可以传播到其他不活跃的突触。 在海马、视觉皮层和杏仁核的突触中观察到的一个例子是，在一组突触处诱导LTP，同时导致周围输入到共享突触后神经元的LTD。 这种同突触LTP和异突触LTD是如何产生的，它们如何相互作用以及它们的功能相关性对于理解学习的细胞基础和一般的适应行为至关重要。 在水蛭中枢神经系统中，在触觉机械感受神经元（T细胞）和S细胞（一种已知对防御性缩短反射的某些学习形式至关重要的中间神经元）之间的突触连接中诱导LTP，也会在非强直性T细胞与同一突触后S细胞形成的突触中产生LTD。 T-S突触处的同突触LTP（homLTP）是NMDA受体非依赖性的，而异突触LTD是NMDA受体依赖性的（Burrell & Sahley，2004）。 这种可塑性模式的一个可能的功能是“调谐”传入输入到突触后细胞，从而改善刺激特异性。 使用水蛭模型系统，我们建议检查的细胞机制，介导homLTP和hetLTD。 此外，我们将研究如何诱导homLTP/hetLTD影响功能输出（动作电位的数量）的S-细胞响应于触摸细胞输入在皮肤上发起。 最后，我们将确定是否homLTP/hetLTD有助于刺激特异性之间的学习和中性刺激在联想学习的缩短反射。 该项目坚持以中心？适应行为的神经机制的主题，因为拟议的实验从介导神经可塑性的细胞过程的研究，这种可塑性在行为水平上对学习的影响。