PUBLICATION

Whole-genome expression profile in zebrafish embryos after chronic exposure to morphine: identification of new genes associated with neuronal function and mu opioid receptor expression

Authors
Herrero-Turrión, M.J., Rodríguez-Martín, I., López-Bellido, R., Rodríguez, R.E.
ID
ZDB-PUB-141009-7
Date
2014
Source
BMC Genomics   15: 874 (Journal)
Registered Authors
Keywords
none
Datasets
GEO:GSE61062
MeSH Terms
  • Neurons/metabolism
  • Signal Transduction/drug effects
  • Embryo, Nonmammalian/anatomy & histology
  • Embryo, Nonmammalian/drug effects
  • Cell Differentiation/drug effects
  • Gene Expression Profiling/methods
  • Morphine/adverse effects*
  • Zebrafish/anatomy & histology
  • Zebrafish/embryology*
  • Gene Expression Regulation, Developmental/drug effects*
  • Animals
  • Oligonucleotide Array Sequence Analysis/methods
  • Chorion/drug effects*
  • Analgesics, Opioid/adverse effects*
  • Receptors, Opioid, mu/genetics*
(all 15)
PubMed
25294025 Full text @ BMC Genomics
Abstract
A great number of studies have investigated changes induced by morphine exposure in gene expression using several experimental models. In this study, we examined gene expression changes during chronic exposure to morphine during maturation and differentiation of zebrafish CNS.
Microarray analysis showed 254 genes whose expression was identified as different by at least 1.3 fold change following chronic morphine exposure as compared to controls. Of these, several novel genes (grb2, copb2, otpb, magi1b, grik-l, bnip4 and sox19b) have been detected for the first time in an experimental animal model treated with morphine. We have also identified a subset of genes (dao.1, wls, bnip4 and camk1gammab) differentially expressed by chronic morphine exposure whose expression is related to mu opioid receptor gene expression. Altered expression of copb2, bnip4, sox19b, otpb, dao.1, grik-l and wls is indicative of modified neuronal development, CNS patterning processes, differentiation and dopaminergic neurotransmission, serotonergic signaling pathway, and glutamatergic neurotransmission. The deregulation of camk1gammab signaling genes suggests an activation of axonogenesis and dendritogenesis.
Our study identified different functional classes of genes and individual candidates involved in the mechanisms underlying susceptibility to morphine actions related to CNS development. These results open new lines to study the treatment of pain and the molecular mechanisms involved in addiction. We also found a set of zebrafish-specific morphine-induced genes, which may be putative targets in human models for addiction and pain processes.
Genes / Markers
Figures
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Expression
Phenotype
No data available
Mutations / Transgenics
No data available
Human Disease / Model
No data available
Sequence Targeting Reagents
Target Reagent Reagent Type
oprm1MO1-oprm1MRPHLNO
1 - 1 of 1
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Fish
1 - 2 of 2
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Antibodies
No data available
Orthology
No data available
Engineered Foreign Genes
No data available
Mapping
No data available