ArticleJournal of medical virology2019
Transgenic increase in the β-endorphin concentration in cerebrospinal fluid alleviates morphine-primed relapse behavior through the μ opioid receptor in rats.
Article in Journal of medical virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Formation of a β-Endorphin Corona Mitigates Alzheimer's Amyloidogenesis.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Kappa Opioid Signaling at the Crossroads of Chronic Pain and Opioid Addiction.Handbook of experimental pharmacology · 2022Article
- A Runner's High for New Neurons? Potential Role for Endorphins in Exercise Effects on Adult Neurogenesis.Biomolecules · 2021Review
- Transgenic increase in the β-endorphin concentration in cerebrospinal fluid alleviates morphine-primed relapse behavior through the μ opioid receptor in rats.Journal of medical virology · 2019Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOpioid-primed relapse is a global burden. Although current strategies have improved, optimal therapy is urgently needed.
methodsA recombinant adenovirus (Ad-NEP) expressing β-endorphin (β-EP) was designed and injected intracerebroventricularly (icv) into the right lateral ventricle in rats. Spatial and temporal β-EP expression in the lateral ventricle wall, subventricular zone and adjacent choroid plexus and the β-EP concentration in the cerebrospinal fluid (CSF) were observed during a 21-day period. A morphine priming-induced conditioned place preference (CPP) rat model was established. The β-EP-ir neuron counts, CSF β-EP concentration, and CPP score, which were used to evaluate morphine-primed reinstatement following extinction, were recorded 7 days after the icv injection. Additionally, the rats were pretreated with the irreversible μ opioid receptor antagonist β-funaltrexamine (β-FNA) and the selective κ opioid receptor antagonist nor-binaltorphimine (nor-BNI) to identify the receptor-dependent mechanism.
resultsBoth peak β-EP expression in target neurons and the peak CSF β-EP concentration occurred 7 to 8 days after Ad-NEP icv injection. The sustainable increase in the CSF β-EP concentration was correlated with a decrease in the CPP score 7 days after the Ad-NEP icv injection. Furthermore, reinstatement was almost reversed by β-FNA pretreatment 24 hours before the behavioral test, but nor-BNI had little effect.
conclusionThe increasing cerebrospinal fluid β-endorphin concentrations showed that the therapeutic effect on opioid relapse occurred predominantly through a μ opioid receptor-dependent mechanism. The Ad-NEP adenovirus can be considered an alternative therapy for opioid relapse.
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