Volianskis Arturas, France Grace, Jensen Morten S, Bortolotto Zuner A, Jane David E, Collingridge Graham L
Center for Synaptic Plasticity, School of Physiology and Pharmacology, University of Bristol, United Kingdom.
Center for Synaptic Plasticity, School of Physiology and Pharmacology, University of Bristol, United Kingdom.
Brain Res. 2015 Sep 24;1621:5-16. doi: 10.1016/j.brainres.2015.01.016. Epub 2015 Jan 22.
N-methyl-D-aspartate receptors (NMDARs) are known for their role in the induction of long-term potentiation (LTP). Here we start by reviewing the early evidence for their role in LTP at CA1 synapses in the hippocampus. We then discuss more recent evidence that NMDAR dependent synaptic plasticity at these synapses can be separated into mechanistically distinct components. An initial phase of the synaptic potentiation, which is generally termed short-term potentiation (STP), decays in an activity-dependent manner and comprises two components that differ in their kinetics and NMDAR subtype dependence. The faster component involves activation of GluN2A and GluN2B subunits whereas the slower component involves activation of GluN2B and GluN2D subunits. The stable phase of potentiation, commonly referred to as LTP, requires activation of primarily triheteromeric NMDARs containing both GluN2A and GluN2B subunits. In new work, we compare STP with a rebound potentiation (RP) that is induced by NMDA application and conclude that they are different phenomena. We also report that NMDAR dependent long-term depression (NMDAR-LTD) is sensitive to a glycine site NMDAR antagonist. We conclude that NMDARs are not synonymous for either LTP or memory. Whilst important for the induction of LTP at many synapses in the CNS, not all forms of LTP require the activation of NMDARs. Furthermore, NMDARs mediate the induction of other forms of synaptic plasticity and are important for synaptic transmission. It is, therefore, not possible to equate NMDARs with LTP though they are intimately linked. This article is part of a Special Issue entitled SI: Brain and Memory.
N-甲基-D-天冬氨酸受体（NMDARs）因其在长时程增强（LTP）诱导中的作用而闻名。在此，我们首先回顾其在海马体CA1突触LTP中作用的早期证据。然后，我们讨论更多近期证据，即这些突触处依赖NMDAR的突触可塑性可分为机制上不同的成分。突触增强的初始阶段，通常称为短时程增强（STP），以活动依赖的方式衰减，包括两个在动力学和NMDAR亚型依赖性方面不同的成分。较快的成分涉及GluN2A和GluN2B亚基的激活，而较慢的成分涉及GluN2B和GluN2D亚基的激活。增强的稳定阶段，通常称为LTP，主要需要同时包含GluN2A和GluN2B亚基的三聚体NMDAR的激活。在新的研究中，我们将STP与由NMDA应用诱导的反弹增强（RP）进行比较，并得出它们是不同现象的结论。我们还报告说，依赖NMDAR的长时程抑制（NMDAR-LTD）对甘氨酸位点NMDAR拮抗剂敏感。我们得出结论，NMDARs既不是LTP也不是记忆的同义词。虽然对中枢神经系统中许多突触处LTP的诱导很重要，但并非所有形式的LTP都需要NMDARs的激活。此外，NMDARs介导其他形式突触可塑性的诱导，并且对突触传递很重要。因此，虽然它们密切相关，但不可能将NMDARs与LTP等同起来。本文是名为“SI：大脑与记忆”的特刊的一部分。
