ArticleScientific reports2016
RACK1 promotes maintenance of morphine-associated memory via activation of an ERK-CREB dependent pathway in hippocampus.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Temporal- and sex-specific changes in proteasome-dependent and independent polyubiquitination in the amygdala during fear memory formation.Learning & memory (Cold Spring Harbor, N.Y.) · 2026Article
- A Duality of Function: An Integrative Model of RACK1 as a Switch Between Translational and Signaling Hubs.International journal of molecular sciences · 2025Review
- Oxycodone, an opioid like the others?Frontiers in psychiatry · 2023Review
- Article
- Morphine-induced RACK1-dependent autophagy in immortalized neuronal cell lines.British journal of pharmacology · 2020Article
- Drug-Induced Conditioned Place Preference and Its Practical Use in Substance Use Disorder Research.Frontiers in behavioral neuroscience · 2020Review
- Long non-coding RNA MEG3 attends to morphine-mediated autophagy of HT22 cells through modulating ERK pathway.Pharmaceutical biology · 2019Article
- Rack1 Controls Parallel Fiber-Purkinje Cell Synaptogenesis and Synaptic Transmission.Frontiers in cellular neuroscience · 2019Article
- Intranasal Lactoferrin Enhances α-Secretase-Dependent Amyloid Precursor Protein Processing via the ERK1/2-CREB and HIF-1α Pathways in an Alzheimer's Disease Mouse Model.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- RACK1 regulates neural development.Neural regeneration research · 2017Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Existence of long-term drug-associated memories may be a crucial factor in drug cravings and relapse. RACK1 plays a critical role in morphine-induced reward. In the present study, we used conditioned place preference (CPP) to assess the acquisition and maintenance of morphine conditioned place preference memory. The hippocampal protein level of RACK1 and synaptic quantitation were evaluated by Western blotting, immunohistochemistry and electron microscopy, respectively. Additionally, shRACK1 (shGnb2l1) was used to silence RACK1 in vivo to evaluate the role and the underlying mechanism of RACK1 in maintenance of morphine CPP memory. We found that morphine induced CPP was maintained for at least 7 days after the last morphine treatment, which indicated a positive correlation with hippocampal RACK1 level, and was accompanied simultaneously by increases in the synapse density and hippocampal expression of synaptophysin (SYP), phosphorylation of extracellular signal-regulated kinase1/2 (pERK1/2) and the phosphorylation of cyclic adenosine monophosphate response element-binding (pCREB). ShGnb2l1 icv injection significantly suppressed the expression of all above proteins, decreased the synapse density in the hippocampus and attenuated the acquisition and maintenance of morphine CPP. Our present study highlights that RACK1 plays an important role in the maintenance of morphine CPP, likely via activation of ERK-CREB pathway in hippocampus.
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