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首页> 外文期刊>Hippocampus >Dopamine D1/D5 Receptor Signaling Regulates Synaptic Cooperation and Competition in Hippocampal CA1 Pyramidal Neurons via Sustained ERK1/2 Activation
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Dopamine D1/D5 Receptor Signaling Regulates Synaptic Cooperation and Competition in Hippocampal CA1 Pyramidal Neurons via Sustained ERK1/2 Activation

机译：多巴胺D1 / D5受体信号传导通过持续的ERK1 / 2激活调节海马CA1锥体神经元的突触合作和竞争。

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Synaptic cooperation and competition are important components of synaptic plasticity that tune synapses for the formation of associative long-term plasticity, a cellular correlate of associative long-term memory. We have recently reported that coincidental activation of weak synapses within the vicinity of potentiated synapses will alter the cooperative state of synapses to a competitive state thus leading to the slow decay of long-term plasticity, but the molecular mechanism underlying this is still unknown. Here, using acute hippocampal slices of rats, we have examined how increasing extracellular dopamine concentrations interact and/or affect electrically induced long-term potentiation (LTP) in the neighboring synapses. We demonstrate that D1/D5-receptor-mediated potentiation at the CA1 Schaffer collateral synapses differentially regulates synaptic co-operation and competition. Further investigating the molecular players involved, we reveal an important role for extracellular signal-regulated kinases-1 and 2 (ERK1/2) as signal integrators and dose-sensors. Interestingly, a sustained activation of ERK1/2 pathway seems to be involved in the differential regulation of synaptic associativity. The concentration-dependent effects of the modulatory transmitter, as demonstrated for dopaminergic signaling in the present study, might offer additional computational power by fine tuning synaptic associativity processes for establishing long-term associative memory in neural networks. (C) 2015 The Authors Hippocampus Published by Wiley Periodicals, Inc.
机译：突触的合作与竞争是突触可塑性的重要组成部分，可调节突触以形成联想的长期可塑性，联想的长期可塑性是细胞的关联。我们最近报道，在增强的突触附近，弱突触的同时激活会将突触的协作状态改变为竞争状态，从而导致长期可塑性的缓慢衰减，但是其潜在的分子机制仍然未知。在这里，我们使用大鼠的急性海马切片，研究了细胞外多巴胺浓度的增加如何相互作用和/或影响邻近突触中的电诱导长期增强（LTP）。我们证明D1 / D5受体介导的CA1 Schaffer侧突触的增强差异调节突触的合作和竞争。进一步调查涉及的分子参与者，我们揭示了细胞外信号调节激酶-1和2（ERK1 / 2）作为信号整合剂和剂量传感器的重要作用。有趣的是，ERK1 / 2途径的持续激活似乎与突触结合性的差异调节有关。如本研究中对多巴胺能信号传导所证实的，调制递质的浓度依赖性效应可能通过微调突触结合过程在神经网络中建立长期联想记忆而提供额外的计算能力。 （C）2015作者海马（Wiley Periodicals，Inc.）

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