ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Hippocampal long-term potentiation is disrupted during expression and extinction but is restored after reinstatement of morphine place preference.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
- Discovery of non-opioid peptides that selectively relieve mechanical pain in rodents through inhibition of TRPV4 channels.Acta pharmacologica Sinica · 2026Article
- Modulation of dorsal hippocampal SK2 channels regulates morphine-enhanced neuronal oscillations and morphine-induced contextual memory encoding and retrieval.Scientific reports · 2025Article
- A synthetic peptide, derived from neurotoxin GsMTx4, acts as a non-opioid analgesic to alleviate mechanical and neuropathic pain through the TRPV4 channel.Acta pharmaceutica Sinica. B · 2025Article
- Effect of Myelopeptide MP5 on Synaptic Plasticity of the Hippocampus during Addictive Memory Extinction in C57BL/6 Mice.Bulletin of experimental biology and medicine · 2025Article
- A locus coeruleus to dorsal hippocampus pathway mediates cue-induced reinstatement of opioid self-administration in male and female rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Role of α1-GABAJournal of psychopharmacology (Oxford, England) · 2024Article
- Dorsal hippocampus to nucleus accumbens projections drive reinforcement via activation of accumbal dynorphin neurons.Nature communications · 2024Article
- Mapping functional traces of opioid memories in the rat brain.Brain communications · 2024Article
- Postpartum scarcity-adversity inflicts sex-specific cerebellar adaptations and reward behaviors in adolescence.Pharmacology, biochemistry, and behavior · 2023Article
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- A Novel CaMKII Inhibitory Peptide Blocks Relapse to Morphine Seeking by Influencing Synaptic Plasticity in the Nucleus Accumbens Shell.Brain sciences · 2022Article
- Kappa-opioid receptor activation reinstates nicotine self-administration in mice.Addiction neuroscience · 2022Article
- Sex and chronic stress alter the distribution of glutamate receptors within rat hippocampal CA3 pyramidal cells following oxycodone conditioned place preference.Neurobiology of stress · 2022Article
- Anterior cingulate cortex and its projections to the ventral tegmental area regulate opioid withdrawal, the formation of opioid context associations and context-induced drug seeking.Frontiers in neuroscience · 2022Article
- Sex Differences in the Role of CNIH3 on Spatial Memory and Synaptic Plasticity.Biological psychiatry · 2021Article
- A Conantokin Peptide Con-T[M8Q] Inhibits Morphine Dependence with High Potency and Low Side Effects.Marine drugs · 2021Article
- Dose-dependent induction of CPP or CPA by intra-pVTA ethanol: Role of mu opioid receptors and effects on NMDA receptors.Progress in neuro-psychopharmacology & biological psychiatry · 2020Article
- Spermidine, a positive modulator of the NMDA receptor, facilitates extinction and prevents the reinstatement of morphine-induced conditioned place preference in mice.Psychopharmacology · 2020Article
- Drug-Induced Conditioned Place Preference and Its Practical Use in Substance Use Disorder Research.Frontiers in behavioral neuroscience · 2020Review
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Abstract
Learned associations between environmental cues and morphine use play an important role in the maintenance and/or relapse of opioid addiction. Although previous studies suggest that context-dependent morphine treatment alters glutamatergic transmission and synaptic plasticity in the hippocampus, their role in morphine conditioned place preference (CPP) and reinstatement remains unknown. We investigated changes in synaptic plasticity and NMDAR expression in the hippocampus after the expression, extinction, and reinstatement of morphine CPP. Here we report that morphine CPP is associated with increased basal synaptic transmission, impaired hippocampal long-term potentiation (LTP), and increased synaptic expression of the NR1 and NR2b NMDAR subunits. Changes in synaptic plasticity, synaptic NR1 and NR2b expression, and morphine CPP were absent when morphine was not paired with a specific context. Furthermore, hippocampal LTP was impaired and synaptic NR2b expression was increased after extinction of morphine CPP, indicating that these alterations in plasticity may be involved in the mechanisms underlying the learning of drug-environment associations. After extinction of morphine CPP, a priming dose of morphine was sufficient to reinstate morphine CPP and was associated with LTP that was indistinguishable from saline control groups. In contrast, morphine CPP extinguished mice that received a saline priming dose did not show CPP and had disrupted hippocampal LTP. Finally, we found that reinstatement of morphine CPP was prevented by the selective blockade of the NR2b subunit in the hippocampus. Together, these data suggest that alterations in synaptic plasticity and glutamatergic transmission play an important role in the reinstatement of morphine CPP.
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