ArticleProceedings of the National Academy of Sciences of the United States of America2015
β-Arrestin-biased signaling mediates memory reconsolidation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 69 citations in OpenAlex.
- Appetitive Pavlovian conditioned approach to reward location is reduced by both adrenergic and NMDA receptor antagonism at memory reconsolidation.Psychopharmacology · 2026Article
- Circuit-informed modulation of traumatic memory in PTSD: integrating extinction, suppression, and reconsolidation.Molecular psychiatry · 2026Review
- The clinical implication of β-arrestins-mediated signaling in memory and cognition.Molecular and cellular biochemistry · 2025Review
- Memory Reconsolidation Updating in Substance Addiction: Applications, Mechanisms, and Future Prospects for Clinical Therapeutics.Neuroscience bulletin · 2025Review
- Single-dose methamphetamine administration impairs ORM retrieval in mice via excessive DA-mediated inhibition of PrLActa pharmacologica Sinica · 2024Article
- Termination of convulsion seizures by destabilizing and perturbing seizure memory engrams.Science advances · 2024Article
- The multifaceted functions of β-arrestins and their therapeutic potential in neurodegenerative diseases.Experimental & molecular medicine · 2024Review
- The hippocampal FTO-BDNF-TrkB pathway is required for novel object recognition memory reconsolidation in mice.Translational psychiatry · 2023Article
- Paternal methamphetamine exposure induces higher sensitivity to methamphetamine in male offspring through driving ADRB1 on CaMKII-positive neurons in mPFC.Translational psychiatry · 2023Article
- Review
- Arrestin-dependent nuclear export of phosphodiesterase 4D promotes GPCR-induced nuclear cAMP signaling required for learning and memory.Science signaling · 2023Article
- Memory Impairing Effect of Propranolol on Consolidation and Reconsolidation for Various Learning Tasks.Noro psikiyatri arsivi · 2023Review
- Noradrenergic consolidation of social recognition memory is mediated by β-arrestin-biased signaling in the mouse prefrontal cortex.Communications biology · 2022Article
- A novel microRNA, novel-m009C, regulates methamphetamine rewarding effects.Molecular psychiatry · 2022Article
- Disrupting reconsolidation by PKA inhibitor in BLA reduces heroin-seeking behavior.Frontiers in cellular neuroscience · 2022Article
- Targeting the Beta-2-Adrenergic Receptor and the Risk of Developing Alzheimer's Disease: A Retrospective Inception Cohort Study.Journal of Alzheimer's disease : JAD · 2022Article
- Mechanisms Underlying Mu Opioid Receptor Effects on Parallel Fiber-Purkinje Cell Synaptic Transmission in Mouse Cerebellar Cortex.Frontiers in synaptic neuroscience · 2022Article
- Dose-Dependent Regulation on Prefrontal Neuronal Working Memory by Dopamine DFrontiers in neuroscience · 2022Article
- Interfering With Contextual Fear Memories by Post-reactivation Administration of Propranolol in Mice: A Series of Null Findings.Frontiers in behavioral neuroscience · 2022Article
- Functional Selectivity of Dopamine DInternational journal of molecular sciences · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A long-standing hypothesis posits that a G protein-coupled signaling pathway mediates β-adrenergic nervous system functions, including learning and memory. Here we report that memory retrieval (reactivation) induces the activation of β1-adrenergic β-arrestin signaling in the brain, which stimulates ERK signaling and protein synthesis, leading to postreactivation memory restabilization. β-Arrestin2-deficient mice exhibit impaired memory reconsolidation in object recognition, Morris water maze, and cocaine-conditioned place preference paradigms. Postreactivation blockade of both brain β-adrenergic Gs protein- and β-arrestin-dependent pathways disrupts memory reconsolidation. Unexpectedly, selective blockade of the Gs/cAMP/PKA signaling but not the β-arrestin/ERK signaling by the biased β-adrenergic ligands does not inhibit reconsolidation. Moreover, the expression of β-arrestin2 in the entorhinal cortex of β-arrestin 2-deficient mice rescues β1-adrenergic ERK signaling and reconsolidation in a G protein pathway-independent manner. We demonstrate that β-arrestin-biased signaling regulates memory reconsolidation and reveal the potential for β-arrestin-biased ligands in the treatment of memory-related disorders.
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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.