ArticleNeurobiology of learning and memory2014
Co-activation of NR2A and NR2B subunits induces resistance to fear extinction.
Article in Neurobiology of learning and memory, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- N-Methyl D-aspartate receptor subunit signaling in fear extinction.Psychopharmacology · 2019Review
- Role of retrosplenial cortex in processing stress-related context memories.Behavioral neuroscience · 2018Review
- JIP1-Mediated JNK Activation Negatively Regulates Synaptic Plasticity and Spatial Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Infralimbic GluN2A-Containing NMDA Receptors Modulate Reconsolidation of Cocaine Self-Administration Memory.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- The Functional and Molecular Properties, Physiological Functions, and Pathophysiological Roles of GluN2A in the Central Nervous System.Molecular neurobiology · 2017Review
- Muscarinic acetylcholine receptors act in synergy to facilitate learning and memory.Learning & memory (Cold Spring Harbor, N.Y.) · 2016Article
- Pharmacology of cognitive enhancers for exposure-based therapy of fear, anxiety and trauma-related disorders.Pharmacology & therapeutics · 2015Review
- Mechanisms to medicines: elucidating neural and molecular substrates of fear extinction to identify novel treatments for anxiety disorders.British journal of pharmacology · 2014Review
- Cdk5 inhibitor roscovitine alleviates neuropathic pain in the dorsal root ganglia by downregulating N-methyl-D-aspartate receptor subunit 2A.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Unpredictable stress is known to profoundly enhance susceptibility to fear and anxiety while reducing the ability to extinguish fear when threat is no longer present. Accordingly, partial aversive reinforcement, via random exposure to footshocks, induces fear that is resistant to extinction. Here we sought to determine the hippocampal mechanisms underlying susceptibility versus resistance to context fear extinction as a result of continuous (CR) and partial (PR) reinforcement, respectively. We focused on N-methyl-D-aspartate receptor (NMDAR) subunits 2A and B (NR2A and NR2B) as well as their downstream signaling effector, extracellular signal-regulated kinase (ERK), based on their critical role in the acquisition and extinction of fear. Pharmacological inactivation of NR2A, but not NR2B, blocked extinction after CR, whereas inactivation of NR2A, NR2B, or both subunits facilitated extinction after PR. The latter finding suggests that co-activation of NR2A and NR2B contributes to persistent fear following PR. In contrast to CR, PR increased membrane levels of ERK and NR2 subunits after the conditioning and extinction sessions, respectively. In parallel, nuclear activation of ERK was significantly reduced after the extinction session. Thus, co-activation and increased surface expression of NR2A and NR2B, possibly mediated by ERK, may cause persistent fear. These findings suggest that patients with post-traumatic stress disorder (PTSD) may benefit from antagonism of specific NR2 subunits.
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