Related Experiment Video
Updated: Jun 7, 2026

Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE
Published on: April 15, 2014
Could the endogenous opioid, morphine, prevent neural stem cell proliferation?
Alireza Shoae-Hassani1, Shiva Sharif, Seyed Abdolreza Mortazavi Tabatabaei
1Research Center for Science and Technology in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Abstract:
In spite of widespread use of morphine to treat pain in patients, little is known about the effects of this opioid on many cells including stem cells. Moreover the studies have been shown controversial results about morphine effects on several kinds of cells. It is well-known that morphine exposure could decrease testosterone levels in brain and spinal cord. Morphine could increase the activity of 5α-redutase, the enzyme that converts testosterone into its respective 5α-redutase derivative dihydrotestosterone (DHT). Also it could increase aromatase activity that converts testosterone to estradiol. Proliferation of neural stem cells was observed in human stem cells after exposure to certain combinations of steroids especially testosterone. On the other hand DHT has negative effect in neural stem cell reproduction. Morphine induces over-expression of p53 gene that could mediate stem cell apoptosis. Therefore we hypothesized that due to reduction in the testosterone levels, elevation in the DHT levels, and over-expression of p53 gene, morphine could prevent neural stem cell proliferation.
Insights
Morphine may hinder neural stem cell proliferation by lowering testosterone, increasing dihydrotestosterone (DHT), and upregulating the p53 gene, potentially impacting stem cell survival.
Area of Science:
- Neuroscience
- Cell Biology
- Pharmacology
Background:
- Morphine is widely used for pain relief, but its effects on stem cells, particularly neural stem cells, are not well understood.
- Existing research on morphine's cellular effects yields controversial results.
- Morphine impacts sex hormone levels, including decreasing testosterone and altering its metabolites, dihydrotestosterone (DHT) and estradiol.
Purpose of the Study:
- To investigate the potential inhibitory effects of morphine on neural stem cell proliferation.
- To explore the mechanisms underlying morphine's impact on neural stem cells, focusing on sex hormone metabolism and gene expression.
Main Methods:
- The study hypothesizes that morphine's effects on testosterone, DHT, and p53 gene expression could inhibit neural stem cell proliferation.
- This involves analyzing the interplay between morphine, sex hormones (testosterone, DHT), and the p53 pathway in neural stem cells.
Main Results:
- Morphine exposure is associated with reduced testosterone levels in the brain and spinal cord.
- Morphine increases the activity of 5α-reductase, leading to higher dihydrotestosterone (DHT) levels.
- Morphine also increases aromatase activity, converting testosterone to estradiol, and induces p53 gene over-expression, which can mediate apoptosis.
Conclusions:
- The combined effects of reduced testosterone, elevated DHT, and p53 over-expression suggest that morphine may prevent neural stem cell proliferation.
- Understanding these mechanisms is crucial for evaluating the safety and efficacy of morphine in contexts involving stem cell function.
Related Concept Videos
Opioid Analgesics: Morphine and Other Natural Cogeners
Mesenchymal Stem Cells
Opioid Receptors: Overview
Regulation of Hematopoietic Stem Cells

