长期增强的持久记忆和n -甲基-d-天冬氨酸受体。

Brain and neuroscience advances Pub Date : 2019-05-21 eCollection Date: 2019-01-01 DOI:10.1177/2398212819848213
Tvp Bliss, G L Collingridge
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引用次数: 24

摘要

在这篇文章中,我们描述了我们参与长期增强研究的早期阶段。我们首先描述在奥斯陆和伦敦进行的早期实验,在那里长期增强首次被表征。我们讨论了谷氨酸受体的分子药理学控制长时程增强及其对应的长时程抑制的诱导和表达的方式。然后,我们继续总结在了解突触可塑性的细胞机制方面取得的非凡进展,这些进展发生在随后的半个世纪。最后,越来越多的证据表明,长期增强功能受损是许多脑部疾病(LToPathies)的核心特征,本文通过几个选定的例子加以说明。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Persistent memories of long-term potentiation and the <i>N</i>-methyl-d-aspartate receptor.

Persistent memories of long-term potentiation and the <i>N</i>-methyl-d-aspartate receptor.

Persistent memories of long-term potentiation and the N-methyl-d-aspartate receptor.

In this article, we describe our involvement in the early days of research into long-term potentiation. We start with a description of the early experiments conducted in Oslo and London where long-term potentiation was first characterised. We discuss the ways in which the molecular pharmacology of glutamate receptors control the induction and expression of long-term potentiation and its counterpart, long-term depression. We then go on to summarise the extraordinary advances in understanding the cellular mechanisms of synaptic plasticity that have taken place in the subsequent half century. Finally, the increasing evidence that impaired long-term potentiation is a core feature of many brain disorders (LToPathies) is addressed by way of a few selected examples.

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