Hippocampal long-term potentiation that is elicited by perforant path stimulation or that occurs in conjunction with spatial learning is tightly controlled by beta-adrenoreceptors and the locus coeruleus.
Hippocampal long-term potentiation that is elicited by perforant path stimulation or that occurs in conjunction with spatial learning is tightly controlled by beta-adrenoreceptors and the locus coeruleus.
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DOI：
10.1002/hipo.22436
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发表时间：
2015-11
期刊：
影响因子：
3.5
通讯作者：
Manahan-Vaughan D
中科院分区：
文献类型：
--
作者：
Hansen N;Manahan-Vaughan D
去甲肾上腺素能系统，驱动蓝斑（LC）激活，在调节和指导海马突触效能的变化中起着关键作用。LC释放去甲肾上腺素以响应新的体验，LC激活导致基于海马的学习增强，并以与空间学习相关的长时程抑制（LTD）和长时程增强（LTP）的形式促进突触可塑性。介导这些作用的主要受体是β-肾上腺素受体。有趣的是，突触可塑性对这种受体的依赖性在海马子场中是不同的，其中在体内CA 1中，LTP而不是LTD需要β肾上腺素受体激活，而在苔藓纤维突触中，LTP和LTD不依赖于这种受体。相比之下，空间学习促进的突触可塑性高度依赖于海马两个亚区的β肾上腺素受体激活。在这里，我们探讨了是否由穿通径（pp）刺激在体内诱导的LTP或由空间学习促进的LTP取决于β肾上腺素受体。我们发现，在两种LTP条件下，拮抗受体使LTP的持久性失效。β肾上腺素受体拮抗作用也阻止了空间学习。值得注意的是，在pp的高频刺激（HFS）之前激活LC可以阻止短时程增强，但不能阻止LTP，以及在pp-HFS诱导的LTP去增强之后激活LC。β肾上腺素受体拮抗作用阻止了这种去电位作用。这些数据表明，在增强的唤醒和学习过程中，由LC释放去甲肾上腺素引起的β-肾上腺素受体激活，包括一种调节和微调LTP持续时间和程度的机制。这可能有助于优化创建一个空间记忆印迹的LTP和LTD的装置。这个过程可以预期支持的特殊作用，齿状回作为一个重要的次区域的轨迹检测和处理海马内的新奇。© 2015 The Authors Hippocampus由Wiley Periodicals，Inc.
The noradrenergic system, driven by locus coeruleus (LC) activation, plays a key role in the regulating and directing of changes in hippocampal synaptic efficacy. The LC releases noradrenaline in response to novel experience and LC activation leads to an enhancement of hippocampus‐based learning, and facilitates synaptic plasticity in the form of long‐term depression (LTD) and long‐term potentiation (LTP) that occur in association with spatial learning. The predominant receptor for mediating these effects is the β‐adrenoreceptor. Interestingly, the dependency of synaptic plasticity on this receptor is different in the hippocampal subfields whereby in the CA1 in vivo, LTP, but not LTD requires β‐adrenoreceptor activation, whereas in the mossy fiber synapse LTP and LTD do not depend on this receptor. By contrast, synaptic plasticity that is facilitated by spatial learning is highly dependent on β‐adrenoreceptor activation in both hippocampal subfields. Here, we explored whether LTP induced by perforant‐path (pp) stimulation in vivo or that is facilitated by spatial learning depends on β‐adrenoreceptors. We found that under both LTP conditions, antagonising the receptors disabled the persistence of LTP. β‐adrenoreceptor‐antagonism also prevented spatial learning. Strikingly, activation of the LC before high‐frequency stimulation (HFS) of the pp prevented short‐term potentiation but not LTP, and LC stimulation after pp‐HFS‐induced depotentiation of LTP. This depotentiation was prevented by β‐adrenoreceptor‐antagonism. These data suggest that β‐adrenoreceptor‐activation, resulting from noradrenaline release from the LC during enhanced arousal and learning, comprises a mechanism whereby the duration and degree of LTP is regulated and fine tuned. This may serve to optimize the creation of a spatial memory engram by means of LTP and LTD. This process can be expected to support the special role of the dentate gyrus as a crucial subregional locus for detecting and processing novelty within the hippocampus. © 2015 The Authors Hippocampus Published by Wiley Periodicals, Inc.
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