Cited by 144Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsNeurotransmitter Receptor Influence on Behavior

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NMDA GluN2A and GluN2B receptors play separate roles in the induction of LTP and LTD in the amygdala and in the acquisition and extinction of conditioned fear

Dalton, Gemma L., Wu, Dong Chuan, Wang, Yu Tian, Floresco, Stan B., Phillips, Anthony G.·2012·Neuropharmacology

DOI 10.1016/j.neuropharm.2011.09.001

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Abstract

Synaptic plasticity mediated by NMDA glutamate receptors is thought to be a primary mechanism underlying the formation of new memories. Activation of GluN2A NMDA receptor subunits may induce long-term potentiation (LTP), whereas low-frequency stimulation of GluN2B receptors induces long-term depression (LTD). In the present study, we show that blockade of GluN2A, but not GluN2B receptors with NVP-AAM077 and Ro25-6981 respectively, prevented LTP of auditory thalamic inputs to the lateral amygdala. Conversely, LTD induction in this pathway was prevented by blockade of GluN2B, but not GluN2A receptors. As this pathway plays a critical role in the acquisition, retrieval and extinction of a learned auditory-cue fear association, we next examined the effects of blockade of GluN2A and GluN2B receptors on the development and retention of a conditioned fear response. Administration of NVP-AAM077, but not Ro25-6981, prior to conditioning disrupted the expression of conditioned fear 24h later. Conversely, Ro25-6981 but not NVP-AAM077 impaired extinction of the conditioned fear response. These data expand on previous work showing that LTP/D in the thalamic-lateral amygdala pathway is dependent on NMDA receptors, by demonstrating selective roles for GluN2A and GluN2B NMDA receptor subunits in LTP and LTD respectively. Furthermore, GluN2A receptor activation and associated LTP may be involved specifically in the initial formation and/or stabilization of a learned fear response, whereas GluN2B receptor activation and associated LTD may facilitate the suppression of Pavlovian fear responses during extinction. This article is part of a Special Issue entitled 'Post-Traumatic Stress Disorder'.

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Authors: Dalton, G. L., Wu, D. C., Wang, Y. T., Floresco, S. B., & Phillips, A. G.
Affiliations: University of British Columbia (CA)
Corresponding author: Floresco, Stan B.
Phillips, Anthony G.
ORCID: Wu, Dong Chuan
Wang, Yu Tian
Floresco, Stan B.
Phillips, Anthony G.
Venue: Neuropharmacology
Publisher: Elsevier BV
Published: 2012-02
Volume: 62
Issue: 2
Pages: 797-806
ISSN: 0028-3908 (ISSN-L)
DOI: 10.1016/j.neuropharm.2011.09.001
OpenAlex: W2089923284
Cited by: 144
References: 70
Citations by year: 2026: 5 · 2025: 10 · 2024: 7 · 2023: 9 · 2022: 8 · 2021: 16 · 2020: 7 · 2019: 6 · 2018: 5 · 2017: 11 · 2016: 13 · 2015: 9 · 2014: 18 · 2013: 13 · 2012: 7
FWCI: 5.02
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuropharmacology (publishedVersion)
PubMed (publishedVersion)
Funders: Michael Smith Health Research BC
Canadian Institutes of Health Research
Natural Sciences and Engineering Research Council of Canada
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords: NMDA receptor subunits, GluN2A, GluN2B, long-term potentiation, long-term depression, lateral amygdala, auditory fear conditioning, fear extinction, NVP-AAM077, Ro 25-6981, synaptic plasticity
MeSH terms: Amygdala, Animals, Association Learning, Conditioning, Classical, Extinction, Psychological, Fear, Male, Quinoxalines, Receptors, N-Methyl-D-Aspartate, Rats, Sprague-Dawley, Long-Term Potentiation, Excitatory Amino Acid Antagonists, Long-Term Synaptic Depression, Rats

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NMDA GluN2A and GluN2B receptors play separate roles in the induction of LTP and LTD in the amygdala and in the acquisition and extinction of conditioned fear

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