ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Distinct roles of NR2A and NR2B cytoplasmic tails in long-term potentiation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
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118 citing papers in PubMed, 214 citations in OpenAlex.
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- Activity-Dependent Internalization of Glun2B-Containing NMDARs Is Required for Synaptic Incorporation of Glun2A and Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Metabotropic NMDAR Signaling Contributes to Sex Differences in Synaptic Plasticity and Episodic Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Mechanisms of NMDA Receptor Inhibition by Biguanide Compounds.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Individual NMDA receptor GluN2 subunit signaling domains differentially regulate the postnatal maturation of hippocampal excitatory synaptic transmission and plasticity but not dendritic morphology.Synapse (New York, N.Y.) · 2024Article
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- Early expression of GluN2A-containing NMDA receptors in a model of fragile X syndrome.Journal of neurophysiology · 2024Article
- Mechanisms of NMDA Receptor Inhibition by Sepimostat-Comparison with Nafamostat and Diarylamidine Compounds.International journal of molecular sciences · 2023Article
- Synaptic memory and CaMKII.Physiological reviews · 2023Review
- Light-Sensitive Open Channel Block of Ionotropic Glutamate Receptors by Quaternary Ammonium Azobenzene Derivatives.International journal of molecular sciences · 2023Article
- GluN2B-NMDAR subunit contribution on synaptic plasticity: A phenomenological model for CA3-CA1 synapses.Frontiers in synaptic neuroscience · 2023Article
- GluN2B-containing NMDARs in the mammalian brain: pharmacology, physiology, and pathology.Frontiers in molecular neuroscience · 2023Review
- Excitatory Synaptic Transmission in Ischemic Stroke: A New Outlet for Classical Neuroprotective Strategies.International journal of molecular sciences · 2022Review
- Apamin structure and pharmacology revisited.Frontiers in pharmacology · 2022Article
- Steroid Receptor Coactivator 3 Regulates Synaptic Plasticity and Hippocampus-dependent Memory.Neuroscience bulletin · 2021Article
- Low-intensity ultrasound restores long-term potentiation and memory in senescent mice through pleiotropic mechanisms including NMDAR signaling.Molecular psychiatry · 2021Article
- Hippocampal network dysfunction as a mechanism of early-onset dementia after preeclampsia and eclampsia.Progress in neurobiology · 2021Article
58 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
NMDA receptors (NMDARs) are critical mediators of activity-dependent synaptic plasticity, but the differential roles of NR2A- versus NR2B-containing NMDARs have been controversial. Here, we investigate the roles of NR2A and NR2B in long-term potentiation (LTP) in organotypic hippocampal slice cultures using RNA interference (RNAi) and overexpression, to complement pharmacological approaches. In young slices, when NR2B is the predominant subunit expressed, LTP is blocked by the NR2B-selective antagonist Ro25-6981 [R-(R,S)-alpha-(4-hydroxyphenyl)-beta-methyl-4-(phenylmethyl)-1-piperidine propranol]. As slices mature and NR2A expression rises, activation of NR2B receptors became no longer necessary for LTP induction. LTP was blocked, however, by RNAi knockdown of NR2B, and this was rescued by coexpression of an RNAi-resistant NR2B (NR2B*) cDNA. Interestingly, a chimeric NR2B subunit in which the C-terminal cytoplasmic tail was replaced by that of NR2A failed to rescue LTP, whereas the reverse chimera, NR2A channel with NR2B tail, was able to restore LTP. Thus, expression of NR2B with its intact cytoplasmic tail is required for LTP induction, at an age when channel activity of NR2B-NMDARs is not required for LTP. Overexpression of wild-type NR2A failed to rescue LTP in neurons transfected with the NR2B-RNAi construct, despite restoring NMDA-EPSC amplitude to a similar level as NR2B*. Surprisingly, an NR2A construct lacking its entire C-terminal cytoplasmic tail regained its ability to restore LTP. Together, these data suggest that the NR2B subunit plays a critical role for LTP, presumably by recruiting relevant molecules important for LTP via its cytoplasmic tail. In contrast, NR2A is not essential for LTP, and its cytoplasmic tail seems to carry inhibitory factors for LTP.
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