Morphine effects on striatal transcriptome in mice

Korostyński, Michał; Piechota, Marcin; Kaminska, Dorota; Solecki, Wojciech; Przewłocki, Ryszard

doi:10.1186/gb-2007-8-6-r128

Cited by 76 publications

(78 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, our microarray analysis, in addition to confirm a number of transcriptional targets of morphine (Korostynski et al, 2007;McClung et al, 2005) and reveal novel ones, provided a short list of candidate genes to have a function in HDACimediated enhancement of non-homeostatic behavioral responses to morphine. Particularly remarkable is the case of circadian clock genes.…”

Section: Discussionmentioning

confidence: 99%

“…Although circadian clock genes are appealing candidates for mediating the interaction between sodium butyrate and morphine, the transcriptional program activated by chronic morphine is broad (Korostynski et al, 2007;McClung et al, 2005) and its interaction with sodium butyrate complex ( Figure 5; Supplementary Figure S5). Besides circadian genes, our results show that morphine and sodium butyrate interact on the regulation of the expression of several other transcription factors that may lead to further transcriptional changes, such as fosB, the activity-regulated transcription factors Npas4 and Nr4al, and the transcriptional repressor Zbtb16 that positively regulates the ERK pathway and can potentially enhance drug effects.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Selective Boosting of Transcriptional and Behavioral Responses to Drugs of Abuse by Histone Deacetylase Inhibition

Sanchis‐Segura

López‐Atalaya

Barco

2009

Neuropsychopharmacol

122

View full text Add to dashboard Cite

Histone acetylation and other modifications of the chromatin are important regulators of gene expression and, consequently, may contribute to drug-induced behaviors and neuroplasticity. Earlier studies have shown that a reduction in histone deacetylase (HDAC) activity results in the enhancement of some psychostimulant-induced behaviors. In this study, we extend those seminal findings by showing that the administration of the HDAC inhibitor sodium butyrate enhances morphine-induced locomotor sensitization and conditioned place preference. In contrast, this compound has no effects on the development of morphine tolerance and dependence. Similar effects were observed for cocaine and ethanol-induced behaviors. These behavioral changes were accompanied by a selective boosting of a component of the transcriptional program activated by chronic morphine administration that included circadian clock genes and other genes relevant to addictive behavior. Our results support a specific function for histone acetylation and the epigenetic modulation of transcription at a reduced number of biologically relevant loci on non-homeostatic, long-lasting, drug-induced behavioral plasticity.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Selective Boosting of Transcriptional and Behavioral Responses to Drugs of Abuse by Histone Deacetylase Inhibition

Sanchis‐Segura

López‐Atalaya

Barco

2009

Neuropsychopharmacol

122

View full text Add to dashboard Cite

show abstract

“…GCs exert their effect primarily by binding to the GR, a transcription factor that interacts with genomic GR-responsive elements (GRE) and acts as a cofactor for other transcription factors. Further support of the role of GCs in mediating the biological effects of morphine can be found in studies indicating that disruption of GC signaling alters the long-term effects of morphine, such as the development of behavioral sensitization (Deroche et al, 1992), physical dependence (Korostynski et al, 2007) and reward learning (see Marinelli and Piazza, 2002;de Jong and de Kloet, 2004;Dong et al, 2006; for review). Several morphine-induced genes that belong to the GR-dependent cluster have been found to be astrocyte-specific, including Gjb6 and Sult1a1 (Cahoy et al, 2008;Piechota et al, 2010b).…”

Section: Introductionmentioning

confidence: 96%

“…This signal causes disinhibition of dopaminergic neurons activity and increases dopamine release in the dorsal and ventral striatum, brain regions that are crucial for the development of addiction, further leading to rearrangement of synaptic connections. Inducing structural plasticity of the neuronal network requires alterations of the transcriptional profile (Ammon-Treiber and Hollt, 2005;Rhodes and Crabbe, 2005;McClung and Nestler, 2008), and our previous studies suggest that some morphineinduced transcriptional effects in the striatum are mediated by glucocorticoid (GC) receptor (GR) activation (Korostynski et al, 2007;Piechota et al, 2010b). This response is most likely due to opioid-induced activation of the hypothalamus-pituitary-adrenal axis, which eventually leads to the release of GCs from the adrenal glands (Suemaru et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Astrocytes are a neural target of morphine action via glucocorticoid receptor‐dependent signaling

Ślęzak

Korostyński

Gieryk

et al. 2013

Glia

Self Cite

View full text Add to dashboard Cite

Chronic opioid use leads to the structural reorganization of neuronal networks, involving genetic reprogramming in neurons and glial cells. Our previous in vivo studies have revealed that a significant fraction of the morphine-induced alterations to the striatal transcriptome included glucocorticoid (GC) receptor (GR)-dependent genes. Additional analyses suggested glial cells to be the locus of these changes. In the current study, we aimed to differentiate the direct transcriptional effects of morphine and a GR agonist on primary striatal neurons and astrocytes. Whole-genome transcriptional profiling revealed that while morphine had no significant effect on gene expression in both cell types, dexamethasone significantly altered the transcriptional profile in astrocytes but not neurons. We obtained a complete dataset of genes undergoing the regulation, which includes genes related to glucose metabolism (Pdk4), circadian activity (Per1) and cell differentiation (Sox2). There was also an overlap between morphine-induced transcripts in striatum and GR-dependent transcripts in cultured astrocytes. We further analyzed the regulation of expression of one gene belonging to both groups, serum and GC regulated kinase 1 (Sgk1). We identified two transcriptional variants of Sgk1 that displayed selective GR-dependent upregulation in cultured astrocytes but not neurons. Moreover, these variants were the only two that were found to be upregulated in vivo by morphine in a GR-dependent fashion. Our data suggest that the morphine-induced, GR-dependent component of transcriptome alterations in the striatum is confined to astrocytes. Identification of this mechanism opens new directions for research on the role of astrocytes in the central effects of opioids. V V C 2013 Wiley Periodicals, Inc.

show abstract

“…This research might provide a promising foundation for determining the effect of acute and chronic morphine treatment at the gene level. (Korostynski et al, 2007), which was obtained from Array Express. This publicly available microarray dataset was used to evaluate DEGs between 12 subjects who were acutely treated with morphine, 12 subjects who were chronically treated with morphine, and 12 normal control subjects.…”

Section: Introductionmentioning

confidence: 99%

Investigation of genes in chronic and acute morphine-treated mice using microarray datasets

Ding¹,

Zhang²,

Yu³

et al. 2015

Genet. Mol. Res.

View full text Add to dashboard Cite

ABSTRACT. Morphine is a psychoactive medication that is used as a standard analgesic treatment to relieve pain in clinics. Many patients rely on chronic or acute treatment of morphine to treat pain. However, morphine is a narcotic and has a reverse effect when inappropriately used. Therefore, it is necessary to study chronic and acute morphine treatment to improve pain relief. In this study, differentially expressed genes of acute and chronic morphine-treated mice were identified using Array Express datasets. The genes that were associated with these two types of morphine treatment are discussed. A co-expression network was constructed, and the hub genes were identified. Gene ontology enrichment analysis and pathway analysis were performed using the Gene Ontology website and Kyoto Encyclopedia of Genes and Genomes, respectively. Our study revealed genes that are associated with acute and chronic morphine treatment. Therefore, this study is L. Ding et al. 10194©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (3): 10193-10205 (2015) potentially useful for improving pain relief of patients by acute and chronic morphine treatment.

show abstract

Morphine effects on striatal transcriptome in mice

Cited by 76 publications

References 58 publications

Selective Boosting of Transcriptional and Behavioral Responses to Drugs of Abuse by Histone Deacetylase Inhibition

Selective Boosting of Transcriptional and Behavioral Responses to Drugs of Abuse by Histone Deacetylase Inhibition

Astrocytes are a neural target of morphine action via glucocorticoid receptor‐dependent signaling

Investigation of genes in chronic and acute morphine-treated mice using microarray datasets

Contact Info

Product

Resources

About