Transcriptional Effects of Psychoactive Drugs on Genes Involved in Neurogenesis

Although neurogenesis is affected in several psychiatric diseases, the effects and mechanisms of action of psychoactive drugs on neurogenesis remain unknown and/or controversial. This study aims to evaluate the effects of psychoactive drugs on the expression of genes involved in neurogenesis. Neuron...

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Published in	International journal of molecular sciences Vol. 21; no. 21; p. 8333
Main Authors	Bortolasci, Chiara C., Spolding, Briana, Kidnapillai, Srisaiyini, Connor, Timothy, Truong, Trang T.T., Liu, Zoe S.J., Panizzutti, Bruna, Richardson, Mark F., Gray, Laura, Berk, Michael, Dean, Olivia M., Walder, Ken
Format	Journal Article
Language	English
Published	Switzerland MDPI 06.11.2020
Subjects	Antipsychotic Agents - therapeutic use Cell Line - drug effects Databases, Genetic Gene Expression - drug effects Gene Ontology Humans Neurogenesis - drug effects Neurogenesis - genetics Psychotropic Drugs - metabolism Psychotropic Drugs - pharmacology SOXB1 Transcription Factors - genetics Transcription, Genetic - drug effects bipolar disorder mental health neuroscience neurogenesis psychiatry schizophrenia psychotropic drugs neurons
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Abstract	Although neurogenesis is affected in several psychiatric diseases, the effects and mechanisms of action of psychoactive drugs on neurogenesis remain unknown and/or controversial. This study aims to evaluate the effects of psychoactive drugs on the expression of genes involved in neurogenesis. Neuronal-like cells (NT2-N) were treated with amisulpride (10 µM), aripiprazole (0.1 µM), clozapine (10 µM), lamotrigine (50 µM), lithium (2.5 mM), quetiapine (50 µM), risperidone (0.1 µM), or valproate (0.5 mM) for 24 h. Genome wide mRNA expression was quantified and analysed using gene set enrichment analysis, with the neurogenesis gene set retrieved from the Gene Ontology database and the Mammalian Adult Neurogenesis Gene Ontology (MANGO) database. Transcription factors that are more likely to regulate these genes were investigated to better understand the biological processes driving neurogenesis. Targeted metabolomics were performed using gas chromatography-mass spectrometry. Six of the eight drugs decreased the expression of genes involved in neurogenesis in both databases. This suggests that acute treatment with these psychoactive drugs negatively regulates the expression of genes involved in neurogenesis in vitro. SOX2 and three of its target genes (CCND1, BMP4, and DKK1) were also decreased after treatment with quetiapine. This can, at least in part, explain the mechanisms by which these drugs decrease neurogenesis at a transcriptional level in vitro. These results were supported by the finding of increased metabolite markers of mature neurons following treatment with most of the drugs tested, suggesting increased proportions of mature relative to immature neurons consistent with reduced neurogenesis.
AbstractList	Although neurogenesis is affected in several psychiatric diseases, the effects and mechanisms of action of psychoactive drugs on neurogenesis remain unknown and/or controversial. This study aims to evaluate the effects of psychoactive drugs on the expression of genes involved in neurogenesis. Neuronal-like cells (NT2-N) were treated with amisulpride (10 µM), aripiprazole (0.1 µM), clozapine (10 µM), lamotrigine (50 µM), lithium (2.5 mM), quetiapine (50 µM), risperidone (0.1 µM), or valproate (0.5 mM) for 24 h. Genome wide mRNA expression was quantified and analysed using gene set enrichment analysis, with the neurogenesis gene set retrieved from the Gene Ontology database and the Mammalian Adult Neurogenesis Gene Ontology (MANGO) database. Transcription factors that are more likely to regulate these genes were investigated to better understand the biological processes driving neurogenesis. Targeted metabolomics were performed using gas chromatography-mass spectrometry. Six of the eight drugs decreased the expression of genes involved in neurogenesis in both databases. This suggests that acute treatment with these psychoactive drugs negatively regulates the expression of genes involved in neurogenesis in vitro. SOX2 and three of its target genes (CCND1, BMP4, and DKK1) were also decreased after treatment with quetiapine. This can, at least in part, explain the mechanisms by which these drugs decrease neurogenesis at a transcriptional level in vitro. These results were supported by the finding of increased metabolite markers of mature neurons following treatment with most of the drugs tested, suggesting increased proportions of mature relative to immature neurons consistent with reduced neurogenesis. Although neurogenesis is affected in several psychiatric diseases, the effects and mechanisms of action of psychoactive drugs on neurogenesis remain unknown and/or controversial. This study aims to evaluate the effects of psychoactive drugs on the expression of genes involved in neurogenesis. Neuronal-like cells (NT2-N) were treated with amisulpride (10 µM), aripiprazole (0.1 µM), clozapine (10 µM), lamotrigine (50 µM), lithium (2.5 mM), quetiapine (50 µM), risperidone (0.1 µM), or valproate (0.5 mM) for 24 h. Genome wide mRNA expression was quantified and analysed using gene set enrichment analysis, with the neurogenesis gene set retrieved from the Gene Ontology database and the Mammalian Adult Neurogenesis Gene Ontology (MANGO) database. Transcription factors that are more likely to regulate these genes were investigated to better understand the biological processes driving neurogenesis. Targeted metabolomics were performed using gas chromatography-mass spectrometry. Six of the eight drugs decreased the expression of genes involved in neurogenesis in both databases. This suggests that acute treatment with these psychoactive drugs negatively regulates the expression of genes involved in neurogenesis in vitro. SOX2 and three of its target genes (CCND1, BMP4, and DKK1) were also decreased after treatment with quetiapine. This can, at least in part, explain the mechanisms by which these drugs decrease neurogenesis at a transcriptional level in vitro. These results were supported by the finding of increased metabolite markers of mature neurons following treatment with most of the drugs tested, suggesting increased proportions of mature relative to immature neurons consistent with reduced neurogenesis.Although neurogenesis is affected in several psychiatric diseases, the effects and mechanisms of action of psychoactive drugs on neurogenesis remain unknown and/or controversial. This study aims to evaluate the effects of psychoactive drugs on the expression of genes involved in neurogenesis. Neuronal-like cells (NT2-N) were treated with amisulpride (10 µM), aripiprazole (0.1 µM), clozapine (10 µM), lamotrigine (50 µM), lithium (2.5 mM), quetiapine (50 µM), risperidone (0.1 µM), or valproate (0.5 mM) for 24 h. Genome wide mRNA expression was quantified and analysed using gene set enrichment analysis, with the neurogenesis gene set retrieved from the Gene Ontology database and the Mammalian Adult Neurogenesis Gene Ontology (MANGO) database. Transcription factors that are more likely to regulate these genes were investigated to better understand the biological processes driving neurogenesis. Targeted metabolomics were performed using gas chromatography-mass spectrometry. Six of the eight drugs decreased the expression of genes involved in neurogenesis in both databases. This suggests that acute treatment with these psychoactive drugs negatively regulates the expression of genes involved in neurogenesis in vitro. SOX2 and three of its target genes (CCND1, BMP4, and DKK1) were also decreased after treatment with quetiapine. This can, at least in part, explain the mechanisms by which these drugs decrease neurogenesis at a transcriptional level in vitro. These results were supported by the finding of increased metabolite markers of mature neurons following treatment with most of the drugs tested, suggesting increased proportions of mature relative to immature neurons consistent with reduced neurogenesis. Although neurogenesis is affected in several psychiatric diseases, the effects and mechanisms of action of psychoactive drugs on neurogenesis remain unknown and/or controversial. This study aims to evaluate the effects of psychoactive drugs on the expression of genes involved in neurogenesis. Neuronal-like cells (NT2-N) were treated with amisulpride (10 µM), aripiprazole (0.1 µM), clozapine (10 µM), lamotrigine (50 µM), lithium (2.5 mM), quetiapine (50 µM), risperidone (0.1 µM), or valproate (0.5 mM) for 24 h. Genome wide mRNA expression was quantified and analysed using gene set enrichment analysis, with the neurogenesis gene set retrieved from the Gene Ontology database and the Mammalian Adult Neurogenesis Gene Ontology (MANGO) database. Transcription factors that are more likely to regulate these genes were investigated to better understand the biological processes driving neurogenesis. Targeted metabolomics were performed using gas chromatography-mass spectrometry. Six of the eight drugs decreased the expression of genes involved in neurogenesis in both databases. This suggests that acute treatment with these psychoactive drugs negatively regulates the expression of genes involved in neurogenesis in vitro. and three of its target genes ( , , and ) were also decreased after treatment with quetiapine. This can, at least in part, explain the mechanisms by which these drugs decrease neurogenesis at a transcriptional level in vitro. These results were supported by the finding of increased metabolite markers of mature neurons following treatment with most of the drugs tested, suggesting increased proportions of mature relative to immature neurons consistent with reduced neurogenesis. Although neurogenesis is affected in several psychiatric diseases, the effects and mechanisms of action of psychoactive drugs on neurogenesis remain unknown and/or controversial. This study aims to evaluate the effects of psychoactive drugs on the expression of genes involved in neurogenesis. Neuronal-like cells (NT2-N) were treated with amisulpride (10 µM), aripiprazole (0.1 µM), clozapine (10 µM), lamotrigine (50 µM), lithium (2.5 mM), quetiapine (50 µM), risperidone (0.1 µM), or valproate (0.5 mM) for 24 h. Genome wide mRNA expression was quantified and analysed using gene set enrichment analysis, with the neurogenesis gene set retrieved from the Gene Ontology database and the Mammalian Adult Neurogenesis Gene Ontology (MANGO) database. Transcription factors that are more likely to regulate these genes were investigated to better understand the biological processes driving neurogenesis. Targeted metabolomics were performed using gas chromatography-mass spectrometry. Six of the eight drugs decreased the expression of genes involved in neurogenesis in both databases. This suggests that acute treatment with these psychoactive drugs negatively regulates the expression of genes involved in neurogenesis in vitro. SOX2 and three of its target genes ( CCND1 , BMP4 , and DKK1 ) were also decreased after treatment with quetiapine. This can, at least in part, explain the mechanisms by which these drugs decrease neurogenesis at a transcriptional level in vitro. These results were supported by the finding of increased metabolite markers of mature neurons following treatment with most of the drugs tested, suggesting increased proportions of mature relative to immature neurons consistent with reduced neurogenesis.
Author	Gray, Laura Spolding, Briana Richardson, Mark F. Dean, Olivia M. Connor, Timothy Panizzutti, Bruna Berk, Michael Kidnapillai, Srisaiyini Walder, Ken Bortolasci, Chiara C. Liu, Zoe S.J. Truong, Trang T.T.
AuthorAffiliation	1 The Institute for Mental and Physical Health and Clinical Translation, Barwon Health, Deakin University, Geelong 3220, Australia; briana.spolding@deakin.edu.au (B.S.); timothy.connor@deakin.edu.au (T.C.); truongtra@deakin.edu.au (T.T.T.T.); zoe.liu@deakin.edu.au (Z.S.J.L.); b.panizzuttiparry@deakin.edu.au (B.P.); l.gray@deakin.edu.au (L.G.); michael.berk@deakin.edu.au (M.B.); o.dean@deakin.edu.au (O.M.D.); ken.walder@deakin.edu.au (K.W.) 2 School of Medicine, Centre for Molecular and Medical Research, Deakin University, Geelong 3220, Australia; srisaiyini.kidnapillai@med.lu.se 5 Centre of Youth Mental Health, University of Melbourne, Parkville 3052, Australia 3 School of Life and Environmental Sciences, Genomics Centre, Deakin University, Geelong 3220, Australia; m.richardson@deakin.edu.au 6 Orygen Youth Health Research Centre, Parkville 3052, Australia 4 Department of Psychiatry, Royal Melbourne Hospital, University of Melbourne, Parkville 3052, Australia 7 Florey Institute for Neuroscien
AuthorAffiliation_xml	– name: 6 Orygen Youth Health Research Centre, Parkville 3052, Australia – name: 1 The Institute for Mental and Physical Health and Clinical Translation, Barwon Health, Deakin University, Geelong 3220, Australia; briana.spolding@deakin.edu.au (B.S.); timothy.connor@deakin.edu.au (T.C.); truongtra@deakin.edu.au (T.T.T.T.); zoe.liu@deakin.edu.au (Z.S.J.L.); b.panizzuttiparry@deakin.edu.au (B.P.); l.gray@deakin.edu.au (L.G.); michael.berk@deakin.edu.au (M.B.); o.dean@deakin.edu.au (O.M.D.); ken.walder@deakin.edu.au (K.W.) – name: 3 School of Life and Environmental Sciences, Genomics Centre, Deakin University, Geelong 3220, Australia; m.richardson@deakin.edu.au – name: 5 Centre of Youth Mental Health, University of Melbourne, Parkville 3052, Australia – name: 4 Department of Psychiatry, Royal Melbourne Hospital, University of Melbourne, Parkville 3052, Australia – name: 2 School of Medicine, Centre for Molecular and Medical Research, Deakin University, Geelong 3220, Australia; srisaiyini.kidnapillai@med.lu.se – name: 7 Florey Institute for Neuroscience and Mental Health, University of Melbourne, Parkville 3052, Australia
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Keywords	bipolar disorder mental health neuroscience neurogenesis psychiatry schizophrenia psychotropic drugs neurons
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Snippet	Although neurogenesis is affected in several psychiatric diseases, the effects and mechanisms of action of psychoactive drugs on neurogenesis remain unknown...
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SubjectTerms	Antipsychotic Agents - therapeutic use Cell Line - drug effects Databases, Genetic Gene Expression - drug effects Gene Ontology Humans Neurogenesis - drug effects Neurogenesis - genetics Psychotropic Drugs - metabolism Psychotropic Drugs - pharmacology SOXB1 Transcription Factors - genetics Transcription, Genetic - drug effects
Title	Transcriptional Effects of Psychoactive Drugs on Genes Involved in Neurogenesis
URI	https://www.ncbi.nlm.nih.gov/pubmed/33172123 https://www.proquest.com/docview/2459627326 https://pubmed.ncbi.nlm.nih.gov/PMC7672551
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