Multiple roles of GluN2B-containing NMDA receptors in synaptic plasticity in juvenile hippocampus.
Multiple roles of GluN2B-containing NMDA receptors in synaptic plasticity in juvenile hippocampus.
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含GluN2B的NMDA受体在幼年海马突触可塑性中的多重作用
DOI：
10.1016/j.neuropharm.2016.08.010
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发表时间：
2017-01
影响因子：
4.7
通讯作者：
Volianskis A
中科院分区：
文献类型：
--
作者：
France G;Fernández-Fernández D;Burnell ES;Irvine MW;Monaghan DT;Jane DE;Bortolotto ZA;Collingridge GL;Volianskis A
在海马CA 1区，N-甲基-D-天冬氨酸受体（NMDARs）介导长时程抑制（LTD）、短时程增强（STP）和长时程增强（LTP）的诱导。所有这些形式的突触可塑性可以很容易地研究在青少年海马切片，但参与特定的NMDAR亚基在这些不同形式的突触可塑性的诱导目前尚不清楚。在这里，使用NVP-AAM 077、Ro 25-6981和UBP 145分别靶向含GluN 2A、2B和2D的NMDAR，我们表明含GluN 2B的NMDAR（GluN 2B）参与了从P14大鼠海马制备的切片中LTD、STP和LTP的诱导。选择性阻断含GluN 2B的二异聚体的Ro浓度（1 μM）能够阻断LTP。它还抑制STP的一种组分，而不影响LTP。更高浓度的Ro（10 μM）也抑制GluN 2 A/B三异源聚体，阻断LTP。UBP 145选择性地抑制STP的Ro敏感组分，而NVP抑制LTP。这些数据与GluN 2 B二异聚体在LTD中的作用、含GluN 2 B和GluN 2D的NMDAR在STP中的作用以及GluN 2 A/B三异聚体在LTP中的作用一致。本文是题为“离子型谷氨酸受体”的特刊的一部分。抑制P14中的GluN 2Bs足以阻断NMDAR-LTD。GluN 2A和GluN 2D亚基不是诱导LTD所必需的。STP的诱导涉及GluN 2B和GluN 2D亚基。LTP的诱导依赖于GluN 2A/2B三异源聚体。
In the CA1 area of the hippocampus N-methyl-d-aspartate receptors (NMDARs) mediate the induction of long-term depression (LTD), short-term potentiation (STP) and long-term potentiation (LTP). All of these forms of synaptic plasticity can be readily studied in juvenile hippocampal slices but the involvement of particular NMDAR subunits in the induction of these different forms of synaptic plasticity is currently unclear. Here, using NVP-AAM077, Ro 25-6981 and UBP145 to target GluN2A-, 2B- and 2D-containing NMDARs respectively, we show that GluN2B-containing NMDARs (GluN2B) are involved in the induction of LTD, STP and LTP in slices prepared from P14 rat hippocampus. A concentration of Ro (1 μM) that selectively blocks GluN2B-containing diheteromers is able to block LTD. It also inhibits a component of STP without affecting LTP. A higher concentration of Ro (10 μM), that also inhibits GluN2A/B triheteromers, blocks LTP. UBP145 selectively inhibits the Ro-sensitive component of STP whereas NVP inhibits LTP. These data are consistent with a role of GluN2B diheretomers in LTD, a role of both GluN2B- and GluN2D- containing NMDARs in STP and a role of GluN2A/B triheteromers in LTP. This article is part of the Special Issue entitled ‘Ionotropic glutamate receptors’. Inhibition of GluN2Bs in P14 is sufficient for blockade of NMDAR-LTD. GluN2A and GluN2D subunits are not required for the induction of LTD. Induction of STP involves GluN2B and GluN2D subunits. Induction of LTP depends on GluN2A/2B triheteromers.
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DOI：
10.1073/pnas.89.10.4363
发表时间：
1992-05-15
影响因子：
11.1
作者：
DUDEK, SM;BEAR, MF
通讯作者：
BEAR, MF
影响因子：
5.5
作者：
AULT, B;EVANS, RH;WATKINS, JC
通讯作者：
WATKINS, JC
影响因子：
16.2
作者：
Barria, A;Malinow, R
通讯作者：
Malinow, R
影响因子：
3.6
作者：
Bartlett, Thomas E.;Lu, Jie;Wang, Yu Tian
通讯作者：
Wang, Yu Tian
影响因子：
7.3
作者：
Irvine, Mark W.;Costa, Blaise M.;Jane, David E.
通讯作者：
Jane, David E.