Transcriptomic study of mouse embryonic neural stem cell differentiation under ethanol treatment.Top 50 up and top 50 down regulated genes from microarray analysis. Fold change uploaded. Study identified 496 differentially expressed, author contacted for full list.
Authors:
Mandal C, Park JH, Choi MR, Kim SH, Badejo AC, Chai JC, Lee YS, Jung KH, Chai YG
Gene Ontology (GO) gene set. This set contains genes that have been annotated to the GO term "response to external biotic stimulus", which is defined as "Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of an external biotic stimulus, an external stimulus caused by, or produced by living things." This gene set was automatically constructed using annotation and ontology data provided by GO and only includes annotations with experimental and curatorial evidence codes (EXP, IDA, IPI, IMP, IGI, IEP, TAS, IC). The transitive closure of this term is taken into account using is_a and part_of relationships. For more information: The Gene Ontology Consortium (GOC), http://geneontology.org This gene set was generated using the GeneWeaver GO loader v. 0.2.12.
Authors:
M Ashburner, CA Ball, JA Blake, D Botstein, H Butler, JM Cherry, AP Davis, K Dolinski, SS Dwight, JT Eppig, MA Harris, DP Hill, L Issel-Tarver, A Kasarskis, S Lewis, JC Matese, JE Richardson, M Ringwald, GM Rubin, G Sherlock
Gene Ontology (GO) gene set. This set contains genes that have been annotated to the GO term "biological_process", which is defined as "A biological process represents a specific objective that the organism is genetically programmed to achieve. Biological processes are often described by their outcome or ending state, e.g., the biological process of cell division results in the creation of two daughter cells (a divided cell) from a single parent cell. A biological process is accomplished by a particular set of molecular functions carried out by specific gene products (or macromolecular complexes), often in a highly regulated manner and in a particular temporal sequence." This gene set was automatically constructed using annotation and ontology data provided by GO and only includes annotations with experimental and curatorial evidence codes (EXP, IDA, IPI, IMP, IGI, IEP, TAS, IC). The transitive closure of this term is taken into account using is_a and part_of relationships. For more information: The Gene Ontology Consortium (GOC), http://geneontology.org This gene set was generated using the GeneWeaver GO loader v. 0.2.12.
Authors:
M Ashburner, CA Ball, JA Blake, D Botstein, H Butler, JM Cherry, AP Davis, K Dolinski, SS Dwight, JT Eppig, MA Harris, DP Hill, L Issel-Tarver, A Kasarskis, S Lewis, JC Matese, JE Richardson, M Ringwald, GM Rubin, G Sherlock
Gene Ontology (GO) gene set. This set contains genes that have been annotated to the GO term "response to biotic stimulus", which is defined as "Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a biotic stimulus, a stimulus caused or produced by a living organism." This gene set was automatically constructed using annotation and ontology data provided by GO and only includes annotations with experimental and curatorial evidence codes (EXP, IDA, IPI, IMP, IGI, IEP, TAS, IC). The transitive closure of this term is taken into account using is_a and part_of relationships. For more information: The Gene Ontology Consortium (GOC), http://geneontology.org This gene set was generated using the GeneWeaver GO loader v. 0.2.12.
Authors:
M Ashburner, CA Ball, JA Blake, D Botstein, H Butler, JM Cherry, AP Davis, K Dolinski, SS Dwight, JT Eppig, MA Harris, DP Hill, L Issel-Tarver, A Kasarskis, S Lewis, JC Matese, JE Richardson, M Ringwald, GM Rubin, G Sherlock
Gene Ontology (GO) gene set. This set contains genes that have been annotated to the GO term "response to external stimulus", which is defined as "Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of an external stimulus." This gene set was automatically constructed using annotation and ontology data provided by GO and only includes annotations with experimental and curatorial evidence codes (EXP, IDA, IPI, IMP, IGI, IEP, TAS, IC). The transitive closure of this term is taken into account using is_a and part_of relationships. For more information: The Gene Ontology Consortium (GOC), http://geneontology.org This gene set was generated using the GeneWeaver GO loader v. 0.2.12.
Authors:
M Ashburner, CA Ball, JA Blake, D Botstein, H Butler, JM Cherry, AP Davis, K Dolinski, SS Dwight, JT Eppig, MA Harris, DP Hill, L Issel-Tarver, A Kasarskis, S Lewis, JC Matese, JE Richardson, M Ringwald, GM Rubin, G Sherlock
Gene Ontology (GO) gene set. This set contains genes that have been annotated to the GO term "response to bacterium", which is defined as "Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a stimulus from a bacterium." This gene set was automatically constructed using annotation and ontology data provided by GO and only includes annotations with experimental and curatorial evidence codes (EXP, IDA, IPI, IMP, IGI, IEP, TAS, IC). The transitive closure of this term is taken into account using is_a and part_of relationships. For more information: The Gene Ontology Consortium (GOC), http://geneontology.org This gene set was generated using the GeneWeaver GO loader v. 0.2.12.
Authors:
M Ashburner, CA Ball, JA Blake, D Botstein, H Butler, JM Cherry, AP Davis, K Dolinski, SS Dwight, JT Eppig, MA Harris, DP Hill, L Issel-Tarver, A Kasarskis, S Lewis, JC Matese, JE Richardson, M Ringwald, GM Rubin, G Sherlock
Gene Ontology (GO) gene set. This set contains genes that have been annotated to the GO term "response to other organism", which is defined as "Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a stimulus from another living organism." This gene set was automatically constructed using annotation and ontology data provided by GO and only includes annotations with experimental and curatorial evidence codes (EXP, IDA, IPI, IMP, IGI, IEP, TAS, IC). The transitive closure of this term is taken into account using is_a and part_of relationships. For more information: The Gene Ontology Consortium (GOC), http://geneontology.org This gene set was generated using the GeneWeaver GO loader v. 0.2.12.
Authors:
M Ashburner, CA Ball, JA Blake, D Botstein, H Butler, JM Cherry, AP Davis, K Dolinski, SS Dwight, JT Eppig, MA Harris, DP Hill, L Issel-Tarver, A Kasarskis, S Lewis, JC Matese, JE Richardson, M Ringwald, GM Rubin, G Sherlock
Gene Ontology (GO) gene set. This set contains genes that have been annotated to the GO term "interspecies interaction between organisms", which is defined as "Any process in which an organism has an effect on an organism of a different species." This gene set was automatically constructed using annotation and ontology data provided by GO and only includes annotations with experimental and curatorial evidence codes (EXP, IDA, IPI, IMP, IGI, IEP, TAS, IC). The transitive closure of this term is taken into account using is_a and part_of relationships. For more information: The Gene Ontology Consortium (GOC), http://geneontology.org This gene set was generated using the GeneWeaver GO loader v. 0.2.12.
Authors:
M Ashburner, CA Ball, JA Blake, D Botstein, H Butler, JM Cherry, AP Davis, K Dolinski, SS Dwight, JT Eppig, MA Harris, DP Hill, L Issel-Tarver, A Kasarskis, S Lewis, JC Matese, JE Richardson, M Ringwald, GM Rubin, G Sherlock
Gene Ontology (GO) gene set. This set contains genes that have been annotated to the GO term "response to stimulus", which is defined as "Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a stimulus. The process begins with detection of the stimulus and ends with a change in state or activity or the cell or organism." This gene set was automatically constructed using annotation and ontology data provided by GO and only includes annotations with experimental and curatorial evidence codes (EXP, IDA, IPI, IMP, IGI, IEP, TAS, IC). The transitive closure of this term is taken into account using is_a and part_of relationships. For more information: The Gene Ontology Consortium (GOC), http://geneontology.org This gene set was generated using the GeneWeaver GO loader v. 0.2.12.
Authors:
M Ashburner, CA Ball, JA Blake, D Botstein, H Butler, JM Cherry, AP Davis, K Dolinski, SS Dwight, JT Eppig, MA Harris, DP Hill, L Issel-Tarver, A Kasarskis, S Lewis, JC Matese, JE Richardson, M Ringwald, GM Rubin, G Sherlock
Transcriptomic analysis of gene expression in the nucleus accumbens somatostatin interneurons of male 8�12-week-old Sst-Cre mice or Sst-Cre x TLG498 (SST-TLG498) mice following repeated cocaine intake. Expression was measured via RNA-seq. Values presented are p-values. Data taken from Supplementary Data 1. Data can be accessed at GEO with accession number: GSE116484.A7
Authors:
Efrain A Ribeiro, Marine Salery, Joseph R Scarpa, Erin S Calipari, Peter J Hamilton, Stacy M Ku, Hope Kronman, Immanuel Purushothaman, Barbara Juarez, Mitra Heshmati, Marie Doyle, Casey Lardner, Dominicka Burek, Ana Strat, Stephen Pirpinias, Ezekiell Mouzon, Ming-Hu Han, Rachael L Neve, Rosemary C Bagot, Andrew Kasarskis, Ja Wook Koo, Eric J Nestler
Alcohol transcriptome changes in mice microglia log2FC
Description:
Microglia are fundamentally important immune cells within the central nervous system (CNS) that respond to environmental challenges to maintain normal physiological processes. Alterations in steady-state cellular function and over-activation of microglia can facilitate the initiation and progression of neuropathological conditions such as Alzheimer’s disease, Multiple Sclerosis, and Major Depressive Disorder. Alcohol consumption disrupts signaling pathways including both innate and adaptive immune responses that are necessary for CNS homeostasis. Coordinate expression of these genes is not ascertained from an admixture of CNS cell-types, underscoring the importance of examining isolated cellular populations to reveal systematic gene expression changes arising from mature microglia. Unbiased RNA-Seq profiling was used to identify gene expression changes in isolated prefrontal cortical microglia in response to recurring bouts of voluntary alcohol drinking behavior. The voluntary ethanol paradigm utilizes long-term consumption ethanol that results in escalated alcohol intake and altered cortical plasticity that is seen in humans. Gene coexpression analysis identified a coordinately regulated group of genes, unique to microglia, that collectively are associated with alcohol consumption. Genes within this group are involved in toll-like receptor signaling and transforming growth factor beta signaling. Network connectivity of this group identified Siglech as a putative hub gene and highlighted the potential importance of proteases in the microglial response to chronic ethanol. In conclusion, we identified a distinctive microglial gene expression signature for neuroimmune responses related to alcohol consumption that provides valuable insight into microglia-specific changes underlying the development of substance abuse, and possibly other CNS disorders.
Authors:
Gizelle M McCarthy, Sean P Farris, Yuri A Blednov, R Adron Harris, R Dayne Mayfield
Alcohol transcriptome changes in mice microglia total homogenate log2FC
Description:
Microglia are fundamentally important immune cells within the central nervous system (CNS) that respond to environmental challenges to maintain normal physiological processes. Alterations in steady-state cellular function and over-activation of microglia can facilitate the initiation and progression of neuropathological conditions such as Alzheimer’s disease, Multiple Sclerosis, and Major Depressive Disorder. Alcohol consumption disrupts signaling pathways including both innate and adaptive immune responses that are necessary for CNS homeostasis. Coordinate expression of these genes is not ascertained from an admixture of CNS cell-types, underscoring the importance of examining isolated cellular populations to reveal systematic gene expression changes arising from mature microglia. Unbiased RNA-Seq profiling was used to identify gene expression changes in isolated prefrontal cortical microglia in response to recurring bouts of voluntary alcohol drinking behavior. The voluntary ethanol paradigm utilizes long-term consumption ethanol that results in escalated alcohol intake and altered cortical plasticity that is seen in humans. Gene coexpression analysis identified a coordinately regulated group of genes, unique to microglia, that collectively are associated with alcohol consumption. Genes within this group are involved in toll-like receptor signaling and transforming growth factor beta signaling. Network connectivity of this group identified Siglech as a putative hub gene and highlighted the potential importance of proteases in the microglial response to chronic ethanol. In conclusion, we identified a distinctive microglial gene expression signature for neuroimmune responses related to alcohol consumption that provides valuable insight into microglia-specific changes underlying the development of substance abuse, and possibly other CNS disorders.
Authors:
Gizelle M McCarthy, Sean P Farris, Yuri A Blednov, R Adron Harris, R Dayne Mayfield
Alcohol transcriptome changes in mice microglia total homogenate p-value
Description:
Microglia are fundamentally important immune cells within the central nervous system (CNS) that respond to environmental challenges to maintain normal physiological processes. Alterations in steady-state cellular function and over-activation of microglia can facilitate the initiation and progression of neuropathological conditions such as Alzheimer’s disease, Multiple Sclerosis, and Major Depressive Disorder. Alcohol consumption disrupts signaling pathways including both innate and adaptive immune responses that are necessary for CNS homeostasis. Coordinate expression of these genes is not ascertained from an admixture of CNS cell-types, underscoring the importance of examining isolated cellular populations to reveal systematic gene expression changes arising from mature microglia. Unbiased RNA-Seq profiling was used to identify gene expression changes in isolated prefrontal cortical microglia in response to recurring bouts of voluntary alcohol drinking behavior. The voluntary ethanol paradigm utilizes long-term consumption ethanol that results in escalated alcohol intake and altered cortical plasticity that is seen in humans. Gene coexpression analysis identified a coordinately regulated group of genes, unique to microglia, that collectively are associated with alcohol consumption. Genes within this group are involved in toll-like receptor signaling and transforming growth factor beta signaling. Network connectivity of this group identified Siglech as a putative hub gene and highlighted the potential importance of proteases in the microglial response to chronic ethanol. In conclusion, we identified a distinctive microglial gene expression signature for neuroimmune responses related to alcohol consumption that provides valuable insight into microglia-specific changes underlying the development of substance abuse, and possibly other CNS disorders.
Authors:
Gizelle M McCarthy, Sean P Farris, Yuri A Blednov, R Adron Harris, R Dayne Mayfield
Analysis using RNA-seq of FACS-purified oligodendrocytes revealed a large cohort of morphine-regulated genes. In addition, to investigate cell-type-specific opioid responses, we performed single-cell RNA sequencing (scRNA-seq) of the nucleus accumbens of mice following acute morphine treatment. Differential expression analysis uncovered unique morphine-dependent transcriptional responses by oligodendrocytes and astrocytes.
Authors:
Denis Avey, Sumithra Sankararaman, Aldrin K Y Yim, Ruteja Barve, Jeffrey Milbrandt, Robi D Mitra
Differential gene expression in brainstems of neonatal mice associated with repeated morphine exposure_logFC
Description:
Neonatal outbred Swiss Webster Cartworth Farms White (CFW) mice were administered morphine (15 mg/kg, s.c.) twice daily from postnatal day 1 (P1) to P14, an approximation of the third trimester of human gestation. Female and male mice underwent behavioral testing on P7 and P14 to determine the impact of opioid exposure on anxiety and pain sensitivity. Ultrasonic vocalizations (USVs) and daily body weights were also recorded. Brainstems containing pons and medulla were collected during morphine withdrawal on P14 for RNA sequencing. Morphine induced weight loss from P2 to P14, which persisted during adolescence (P21) and adulthood (P50). USVs markedly increased at P7 in females, emerging earlier than males. On P7 and P14, both morphine-exposed female and male mice displayed hyperalgesia on the hot plate and tail-flick assays, with females showing greater hyperalgesia than males. Morphine-exposed mice exhibited increased anxiety-like behavior in the open-field arena on P21. Transcriptome analysis of the brainstem, an area implicated in opioid withdrawal and NOWS, identified pathways enriched for noradrenergic signaling in females and males. We also found sex-specific pathways related to mitochondrial function and neurodevelopment in females and circadian entrainment in males.
Differential gene expression in brainstems of neonatal female mice associated with repeated morphine exposure_logFC
Description:
Neonatal outbred Swiss Webster Cartworth Farms White (CFW) mice were administered morphine (15 mg/kg, s.c.) twice daily from postnatal day 1 (P1) to P14, an approximation of the third trimester of human gestation. Female and male mice underwent behavioral testing on P7 and P14 to determine the impact of opioid exposure on anxiety and pain sensitivity. Ultrasonic vocalizations (USVs) and daily body weights were also recorded. Brainstems containing pons and medulla were collected during morphine withdrawal on P14 for RNA sequencing. Morphine induced weight loss from P2 to P14, which persisted during adolescence (P21) and adulthood (P50). USVs markedly increased at P7 in females, emerging earlier than males. On P7 and P14, both morphine-exposed female and male mice displayed hyperalgesia on the hot plate and tail-flick assays, with females showing greater hyperalgesia than males. Morphine-exposed mice exhibited increased anxiety-like behavior in the open-field arena on P21. Transcriptome analysis of the brainstem, an area implicated in opioid withdrawal and NOWS, identified pathways enriched for noradrenergic signaling in females and males. We also found sex-specific pathways related to mitochondrial function and neurodevelopment in females and circadian entrainment in males.
Differential gene expression in brainstems of neonatal female mice associated with repeated morphine exposure_pvalue
Description:
Neonatal outbred Swiss Webster Cartworth Farms White (CFW) mice were administered morphine (15 mg/kg, s.c.) twice daily from postnatal day 1 (P1) to P14, an approximation of the third trimester of human gestation. Female and male mice underwent behavioral testing on P7 and P14 to determine the impact of opioid exposure on anxiety and pain sensitivity. Ultrasonic vocalizations (USVs) and daily body weights were also recorded. Brainstems containing pons and medulla were collected during morphine withdrawal on P14 for RNA sequencing. Morphine induced weight loss from P2 to P14, which persisted during adolescence (P21) and adulthood (P50). USVs markedly increased at P7 in females, emerging earlier than males. On P7 and P14, both morphine-exposed female and male mice displayed hyperalgesia on the hot plate and tail-flick assays, with females showing greater hyperalgesia than males. Morphine-exposed mice exhibited increased anxiety-like behavior in the open-field arena on P21. Transcriptome analysis of the brainstem, an area implicated in opioid withdrawal and NOWS, identified pathways enriched for noradrenergic signaling in females and males. We also found sex-specific pathways related to mitochondrial function and neurodevelopment in females and circadian entrainment in males.
Differential gene expression in brainstems of neonatal male mice associated with repeated morphine exposure_logFC
Description:
Neonatal outbred Swiss Webster Cartworth Farms White (CFW) mice were administered morphine (15 mg/kg, s.c.) twice daily from postnatal day 1 (P1) to P14, an approximation of the third trimester of human gestation. Female and male mice underwent behavioral testing on P7 and P14 to determine the impact of opioid exposure on anxiety and pain sensitivity. Ultrasonic vocalizations (USVs) and daily body weights were also recorded. Brainstems containing pons and medulla were collected during morphine withdrawal on P14 for RNA sequencing. Morphine induced weight loss from P2 to P14, which persisted during adolescence (P21) and adulthood (P50). USVs markedly increased at P7 in females, emerging earlier than males. On P7 and P14, both morphine-exposed female and male mice displayed hyperalgesia on the hot plate and tail-flick assays, with females showing greater hyperalgesia than males. Morphine-exposed mice exhibited increased anxiety-like behavior in the open-field arena on P21. Transcriptome analysis of the brainstem, an area implicated in opioid withdrawal and NOWS, identified pathways enriched for noradrenergic signaling in females and males. We also found sex-specific pathways related to mitochondrial function and neurodevelopment in females and circadian entrainment in males.
Differential gene expression in brainstems of neonatal mice associated with repeated morphine exposure_pvalue
Description:
Neonatal outbred Swiss Webster Cartworth Farms White (CFW) mice were administered morphine (15 mg/kg, s.c.) twice daily from postnatal day 1 (P1) to P14, an approximation of the third trimester of human gestation. Female and male mice underwent behavioral testing on P7 and P14 to determine the impact of opioid exposure on anxiety and pain sensitivity. Ultrasonic vocalizations (USVs) and daily body weights were also recorded. Brainstems containing pons and medulla were collected during morphine withdrawal on P14 for RNA sequencing. Morphine induced weight loss from P2 to P14, which persisted during adolescence (P21) and adulthood (P50). USVs markedly increased at P7 in females, emerging earlier than males. On P7 and P14, both morphine-exposed female and male mice displayed hyperalgesia on the hot plate and tail-flick assays, with females showing greater hyperalgesia than males. Morphine-exposed mice exhibited increased anxiety-like behavior in the open-field arena on P21. Transcriptome analysis of the brainstem, an area implicated in opioid withdrawal and NOWS, identified pathways enriched for noradrenergic signaling in females and males. We also found sex-specific pathways related to mitochondrial function and neurodevelopment in females and circadian entrainment in males.
Sig. DEG mouse PFC endothelial cells P21 vs. P60_pvalue
Description:
We performed single cell RNA sequencing (scRNA-seq) to classify all neuron subtypes in prefrontal cortex (PFC) of adolescent (P21) (N = 4) and adult (P60) (N = 12) male C57BL/6 mice (strain mentioned but not explicit in publication) to characterize the transcriptional changes associated with this period (P21-P60). 12 independent biological replicates were used for each age. Each biological replicate was generated by pooling brain tissue from two mice (see methods for more info). To detect similar populations and identify corresponding cell clusters between the 10,646 P21 cells and the 11, 886 P60 PFC cells, we aligned the two scRNA-seq data sets in t-SNE by cross-correlation analysis (CCA)17 (Fig. (Fig.4a).4a). Using bootstrapped correlation, all clusters identified in the adult PFC are detected in the P21 PFC. Based on the expression of cell type-specific markers, the non-neuronal cells were clustered as: astrocytes (Gja1+), oligodendrocyte (Aspa+), newly formed (NF) oligodendrocytes (Bmp4+), oligodendrocyte precursors (OPC) (Pdgfra+), microglia (C1qa+) and endothelial cells (Flt1+) (Fig. 1c, d). The neurons express Snap25 and can be divided into excitatory (Slc17a7+) and inhibitory (Gad2+) neurons (Fig. 1c, d). We then analyzed transcriptional dynamics in each of the neuron subtypes between adolescence (P21) and adulthood (P60) in mouse. The differentially expressed genes between P21 and P60 cells for each cluster was performed using the “FindMarkers” function from the Seurat package using a likelihood ratio test and correcting for the number of detected unique molecular identifier (UMI) bias. Genelists contain significantly differentiated genes in each cell population cluster with fold change > 1.5 and p < 0.05.
Authors:
Aritra Bhattacherjee, Mohamed Nadhir Djekidel, Renchao Chen, Wenqiang Chen, Luis M Tuesta, Yi Zhang
Sig. DEG mouse PFC endothelial cells P21 vs. P60_logFC
Description:
We performed single cell RNA sequencing (scRNA-seq) to classify all neuron subtypes in prefrontal cortex (PFC) of adolescent (P21) (N = 4) and adult (P60) (N = 12) male C57BL/6 mice (strain mentioned but not explicit in publication) to characterize the transcriptional changes associated with this period (P21-P60). 12 independent biological replicates were used for each age. Each biological replicate was generated by pooling brain tissue from two mice (see methods for more info). To detect similar populations and identify corresponding cell clusters between the 10,646 P21 cells and the 11, 886 P60 PFC cells, we aligned the two scRNA-seq data sets in t-SNE by cross-correlation analysis (CCA)17 (Fig. (Fig.4a).4a). Using bootstrapped correlation, all clusters identified in the adult PFC are detected in the P21 PFC. Based on the expression of cell type-specific markers, the non-neuronal cells were clustered as: astrocytes (Gja1+), oligodendrocyte (Aspa+), newly formed (NF) oligodendrocytes (Bmp4+), oligodendrocyte precursors (OPC) (Pdgfra+), microglia (C1qa+) and endothelial cells (Flt1+) (Fig. 1c, d). The neurons express Snap25 and can be divided into excitatory (Slc17a7+) and inhibitory (Gad2+) neurons (Fig. 1c, d). We then analyzed transcriptional dynamics in each of the neuron subtypes between adolescence (P21) and adulthood (P60) in mouse. The differentially expressed genes between P21 and P60 cells for each cluster was performed using the “FindMarkers” function from the Seurat package using a likelihood ratio test and correcting for the number of detected unique molecular identifier (UMI) bias. Genelists contain significantly differentiated genes in each cell population cluster with fold change > 1.5 and p < 0.05.
Authors:
Aritra Bhattacherjee, Mohamed Nadhir Djekidel, Renchao Chen, Wenqiang Chen, Luis M Tuesta, Yi Zhang
Gene expression mouse BLA pattern C CC vs S24_pvalue
Description:
RNA-seq was performed on PFC, dorsal striatum (DStr), NAc, basolateral amygdala (BLA), ventral hippocampus (vHIP), and VTA, obtained from the following six groups of male C57BL/6J mice (Figure 1A): saline SA + 24 hr withdrawal (WD) (S24, n=5–8); cocaine SA + 24 hr WD (C24, n=5–8); saline SA + 30 d WD + saline re-exposure (SS, n=5–8); saline SA + 30 d WD + cocaine exposure (SC, n=5–8); cocaine SA + 30 d WD + saline exposure (CS, n=3–7); and cocaine SA + 30 d WD + cocaine re-exposure (CC, n=5–7). To focus on genes that were uniquely altered following context/drug re-exposure after WD, we compared all groups to the same baseline (S24). We focused on three patterns associated with drug use: first-ever exposure to cocaine (SC; Pattern A; Figure 2B), re-exposure to cocaine-paired context (CS, Pattern B, Figure 2C), and re-exposure to cocaine-paired context + cocaine (CC, Pattern C, Figure 2D). Each Pattern includes genes that were both differentially expressed from S24 (p<0.05; fold change>15%) and distinct from all other groups. The pattern C genes were significantly differentially expressed (see above) between the cocaine SA with cocaine re-exposure after 30 days and baseline (i.e. CC vs S4). Differential expression of the pattern C genes are presented for each group (C24 vs S24, SS vs S4, SC vs S4, CS vs S4, and CC vs S4).
Authors:
Deena M Walker, Hannah M Cates, Yong-Hwee E Loh, Immanuel Purushothaman, Aarthi Ramakrishnan, Kelly M Cahill, Casey K Lardner, Arthur Godino, Hope G Kronman, Jacqui Rabkin, Zachary S Lorsch, Philipp Mews, Marie A Doyle, Jian Feng, Benoit Labonté, Ja Wook Koo, Rosemary C Bagot, Ryan W Logan, Marianne L Seney, Erin S Calipari, Li Shen, Eric J Nestler
GeneWeaver