ArticleBiological psychiatry2016
Naltrexone Facilitates Learning and Delays Extinction by Increasing AMPA Receptor Phosphorylation and Membrane Insertion.
Article in Biological psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Transaldolase 1 contributes to pentose phosphate pathway disruption and synaptic dysfunction in Alzheimer's disease.Translational neurodegeneration · 2026Article
- Investigating pharmacotherapies for alcohol use disorder using Drosophila melanogaster.Alcohol, clinical & experimental research · 2025Article
- Social hierarchy modulates drug reinforcement and protein phosphorylation in the nucleus accumbens.Frontiers in pharmacology · 2025Article
- p85S6K sustains synaptic GluA1 to ameliorate cognitive deficits in Alzheimer's disease.Translational neurodegeneration · 2023Article
- The Role of the Endogenous Opioid System in the Vocal Behavior of Songbirds and Its Possible Role in Vocal Learning.Frontiers in physiology · 2022Review
- Saccharin and naltrexone prevent increased pain sensitivity and impaired long-term memory induced by repetitive neonatal noxious stimulation: role of BDNF and enkephalin.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Naloxone Facilitates Contextual Learning and Memory in a Receptor-Independent and Tet1-Dependent Manner.Cellular and molecular neurobiology · 2021Article
- Glutamatergic Systems and Memory Mechanisms Underlying Opioid Addiction.Cold Spring Harbor perspectives in medicine · 2021Review
- Pre-training naltrexone increases conditioned fear learning independent of adolescent alcohol consumption history.Physiology & behavior · 2021Article
- Calcineurin Participation in Hebbian and Homeostatic Plasticity Associated With Extinction.Frontiers in cellular neuroscience · 2021Review
- PKC and Ras are Involved in M1 Muscarinic Receptor-Mediated Modulation of AMPA Receptor GluA1 Subunit.Cellular and molecular neurobiology · 2020Article
- Acute Stress Facilitates LTD Induction at Glutamatergic Synapses in the Hippocampal CA1 Region by Activating μ-Opioid Receptors on GABAergic Neurons.Frontiers in neuroscience · 2019Article
- Non-nociceptive roles of opioids in the CNS: opioids' effects on neurogenesis, learning, memory and affect.Nature reviews. Neuroscience · 2019Review
- Morphine regulates adult neurogenesis and contextual memory extinction via the PKCε/Prox1 pathway.Neuropharmacology · 2018Article
- Changes in hippocampal AMPA receptors and cognitive impairments in chronic ketamine addiction models: another understanding of ketamine CNS toxicity.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe opioid antagonists naloxone/naltrexone are involved in improving learning and memory, but their cellular and molecular mechanisms remain unknown. We investigated the effect of naloxone/naltrexone on hippocampal α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) trafficking, a molecular substrate of learning and memory, as a probable mechanism for the antagonists activity.
methodsTo measure naloxone/naltrexone-regulated AMPAR trafficking, pHluorin-GluA1 imaging and biochemical analyses were performed on primary hippocampal neurons. To establish the in vivo role of GluA1-Serine 845 (S845) phosphorylation on the behavioral effect induced by inhibition of the endogenous μ-opioid receptor (MOR) by naltrexone, MOR knockout, and GluA1-S845A mutant (in which Ser(845) was mutated to Ala) mice were tested in a water maze after chronic naltrexone administration. Behavioral responses and GluA1 levels in the hippocampal postsynaptic density in wild-type and GluA1-S845A mutant mice were compared using western blot analysis.
resultsIn vitro prolonged naloxone/naltrexone exposure significantly increased synaptic and extrasynaptic GluA1 membrane expression as well as GluA1-S845 phosphorylation. In the MOR knockout and GluA1-S845A mutant mice, naltrexone did not improve learning, which suggests that naltrexone acts via inhibition of endogenous MOR action and alteration of GluA1 phosphorylation. Naltrexone-treated wild-type mice had significantly increased phosphorylated GluA1-S845 and GluA1 levels in their hippocampal postsynaptic density on the third day of acquisition, which is the time when naltrexone significantly improved learning.
conclusionsThe beneficial effect of naltrexone on spatial learning and memory under normal conditions appears to be the result of increasing GluA1-S845 phosphorylation-dependent AMPAR trafficking. These results can be further explored in a mouse model of memory loss.
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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.