ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014
Delayed noradrenergic activation in the dorsal hippocampus promotes the long-term persistence of extinguished fear.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Fear extinction induces maladaptive generalization via noradrenergic and GABAergic systems.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A behavioral tagging account of kinase contribution to memory formation after spaced aversive training.iScience · 2023Article
- Anxiety and hippocampal neuronal activity: Relationship and potential mechanisms.Cognitive, affective & behavioral neuroscience · 2022Review
- TAAR1 regulates drug-induced reinstatement of cocaine-seeking via negatively modulating CaMKIIα activity in the NAc.Molecular psychiatry · 2022Article
- Interleukin-1 receptor-associated kinase 4 (IRAK4) in the nucleus accumbens regulates opioid-seeking behavior in male rats.Brain, behavior, and immunity · 2022Article
- Serotonin 5-HTInternational journal of molecular sciences · 2019Article
- Common neurocircuitry mediating drug and fear relapse in preclinical models.Psychopharmacology · 2019Review
- Effects of Noradrenergic Stimulation Upon Context-Related Extinction Learning Performance and BOLD Activation in Hippocampus and Prefrontal Cortex Differ Between Participants Showing and Not Showing Renewal.Frontiers in behavioral neuroscience · 2019Article
- Role of trace amine-associated receptor 1 in nicotine's behavioral and neurochemical effects.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- Noradrenergic Modulation of Fear Conditioning and Extinction.Frontiers in behavioral neuroscience · 2018Review
- Calpain-GRIP Signaling in Nucleus Accumbens Core Mediates the Reconsolidation of Drug Reward Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Predictable Chronic Mild Stress during Adolescence Promotes Fear Memory Extinction in Adulthood.Scientific reports · 2017Article
- AMPK signaling in the nucleus accumbens core mediates cue-induced reinstatement of cocaine seeking.Scientific reports · 2017Article
- Role of TAAR1 within the Subregions of the Mesocorticolimbic Dopaminergic System in Cocaine-Seeking Behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- EphB2 in the Medial Prefrontal Cortex Regulates Vulnerability to Stress.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- AMPK Signaling in the Dorsal Hippocampus Negatively Regulates Contextual Fear Memory Formation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Overexpression of SIRT6 in the hippocampal CA1 impairs the formation of long-term contextual fear memory.Scientific reports · 2016Article
- Article
- Role of hippocampal β-adrenergic and glucocorticoid receptors in the novelty-induced enhancement of fear extinction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Modulation of Fear Extinction by Stress, Stress Hormones and Estradiol: A Review.Frontiers in behavioral neuroscience · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fear extinction has been extensively studied, but little is known about the molecular processes that underlie the persistence of extinction long-term memory (LTM). We found that microinfusion of norepinephrine (NE) into the CA1 area of the dorsal hippocampus during the early phase (0 h) after extinction enhanced extinction LTM at 2 and 14 days after extinction. Intra-CA1 infusion of NE during the late phase (12 h) after extinction selectively promoted extinction LTM at 14 days after extinction that was blocked by the β-receptor antagonist propranolol, protein kinase A (PKA) inhibitor Rp-cAMPS, and protein synthesis inhibitors anisomycin and emetine. The phosphorylation levels of PKA, cyclic adenosine monophosphate response element-binding protein (CREB), GluR1, and the membrane GluR1 level were increased by NE during the late phase after extinction that was also blocked by propranolol and Rp-cAMPS. These results suggest that the enhancement of extinction LTM persistence induced by NE requires the activation of the β-receptor/PKA/CREB signaling pathway and membrane GluR1 trafficking. Moreover, extinction increased the phosphorylation levels of Erk1/2, CREB, and GluR1, and the membrane GluR1 level during the late phase, and anisomycin/emetine alone disrupted the persistence of extinction LTM, indicating that the persistence of extinction LTM requires late-phase protein synthesis in the CA1. Propranolol and Rp-cAMPS did not completely disrupt the persistence of extinction LTM, suggesting that another β-receptor/PKA-independent mechanism underlies the persistence of extinction LTM. Altogether, our results showed that enhancing hippocampal noradrenergic activity during the late phase after extinction selectively promotes the persistence of extinction LTM.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.