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
  • Analgesics, Opioid/adverse effects*
  • Animals
  • Cell Differentiation/drug effects
  • Chorion/drug effects*
  • Embryo, Nonmammalian/anatomy & histology
  • Embryo, Nonmammalian/drug effects
  • Gene Expression Profiling/methods
  • Gene Expression Regulation, Developmental/drug effects*
  • Morphine/adverse effects*
  • Neurons/metabolism
  • Oligonucleotide Array Sequence Analysis/methods
  • Receptors, Opioid, mu/genetics*
  • Signal Transduction/drug effects
  • Zebrafish/anatomy & histology
  • Zebrafish/embryology*
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
Show all Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes