Activation of the mesolimbic dopamine reward pathway by acute ethanol produces reinforcement and changes in gene expression that appear to be crucial to the molecular basis for adaptive behaviors and addiction. The inbred mouse strains DBA/2J and C57BL/6J exhibit contrasting acute behavioral responses to ethanol. We used oligonucleotide microarrays and bioinformatics methods to characterize patterns of gene expression in three brain regions of the mesolimbic reward pathway of these strains. Expression profiling included examination of both differences in gene expression 4 h after saline injection or acute ethanol (2 g/kg). Using a rigorous stepwise method for microarray analysis, we identified 788 genes differentially expressed in control DBA/2J versus C57BL/6J mice and 307 ethanol-regulated genes in the nucleus accumbens, prefrontal cortex, and ventral tegmental area. There were strikingly divergent patterns of ethanol-responsive gene expression in the two strains. Ethanol-responsive genes also showed clustering at discrete chromosomal regions, suggesting local chromatin effects in regulation. Ethanol-regulated genes were generally related to neuroplasticity, but regulation of discrete functional groups and pathways was brain region specific: glucocorticoid signaling, neurogenesis, and myelination in the prefrontal cortex; neuropeptide signaling and developmental genes, including factor Bdnf, in the nucleus accumbens; and retinoic acid signaling in the ventral tegmental area. Bioinformatics analysis identified several potential candidate genes for quantitative trait loci linked to ethanol behaviors, further supporting a role for expression profiling in identifying genes for complex traits. Brain region-specific changes in signaling and neuronal plasticity may be critical components in development of lasting ethanol behavioral phenotypes such as dependence, sensitization, and craving.
Using a two-stage process, several genes were initially identified using microarray analyses of cerebellar tissue from ethanol-treated PKCgamma mutant and wild-type mice. This geneset consists of genes related to PKCgamma mutant expression changes due to chronic ethanol diet.
Authors:
Bowers BJ, Radcliffe RA, Smith AM, Miyamoto-Ditmon J, Wehner JM
This gene set comprises 17 ethanol-dependence genes that were downregulated in the PKC-gamma wild-type mice during the experiment. Background: Study shows that PKC-gamma wild-type mice develop tolerance to the sedative-hypnotic effects of ethanol after chronic ethanol treatment but mutant mice do not, making these genotypes a suitable model for identifying changes in gene expression related developing tolerance toward ethanol.
Authors:
Bowers BJ, Radcliffe RA, Smith AM, Miyamoto-Ditmon J, Wehner JM
A list of the 307 genes found to be upregulated or downregulated by ethanol in PFC, VTA or NA of B6 or D2 mice. ID number represents cluster membership from Figure 4.
Authors:
Kerns RT, Ravindranathan A, Hassan S, Cage MP, York T, Sikela JM, Williams RW, Miles MF
QTL associated with activity response to ethanol 4. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (118267803)
Authors:
Kerns RT, Ravindranathan A, Hassan S, Cage MP, York T, Sikela JM, Williams RW, Miles MF
12 genes analyzed by PCR from 10 regions of the brains of male Wistar rats following morphine or saline administration. Data taken from Table 3. Values presented are "1" for presence.
Authors:
Timothy M Barrow, Hyang-Min Byun, Xinyan Li, Chris Smart, Yong-Xiang Wang, Yacong Zhang, Andrea A Baccarelli, Liqiong Guo
A member of the nerve growth factor family of trophic factors. In the brain BDNF has a trophic action on retinal, cholinergic, and dopaminergic neurons, and in the peripheral nervous system it acts on both motor and sensory neurons. (From Kendrew, The Encyclopedia of Molecular Biology, 1994)
Generated by gene2mesh v. 1.1.1
GWAS: coffee consumption, cups of coffee per day measurement
Description:
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Coffee consumption (cups per day). The EFO term coffee consumption, cups of coffee per day measurement was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
MC Cornelis, EM Byrne, T Esko, MA Nalls, A Ganna, N Paynter, KL Monda, N Amin, K Fischer, F Renstrom, JS Ngwa, V Huikari, A Cavadino, IM Nolte, A Teumer, K Yu, P Marques-Vidal, R Rawal, A Manichaikul, MK Wojczynski, JM Vink, JH Zhao, G Burlutsky, J Lahti, V Mikkilä, RN Lemaitre, J Eriksson, SK Musani, T Tanaka, F Geller, J Luan, J Hui, R Mägi, M Dimitriou, ME Garcia, WK Ho, MJ Wright, LM Rose, PK Magnusson, NL Pedersen, D Couper, BA Oostra, A Hofman, MA Ikram, HW Tiemeier, AG Uitterlinden, FJ van Rooij, I Barroso, I Johansson, L Xue, M Kaakinen, L Milani, C Power, H Snieder, RP Stolk, SE Baumeister, R Biffar, F Gu, F Bastardot, Z Kutalik, DR Jacobs, NG Forouhi, E Mihailov, L Lind, C Lindgren, K Michaëlsson, A Morris, M Jensen, KT Khaw, RN Luben, JJ Wang, S Männistö, MM Perälä, M Kähönen, T Lehtimäki, J Viikari, D Mozaffarian, K Mukamal, BM Psaty, A Döring, AC Heath, GW Montgomery, N Dahmen, T Carithers, KL Tucker, L Ferrucci, HA Boyd, M Melbye, JL Treur, D Mellström, JJ Hottenga, I Prokopenko, A Tönjes, P Deloukas, S Kanoni, M Lorentzon, DK Houston, Y Liu, J Danesh, A Rasheed, MA Mason, AB Zonderman, L Franke, BS Kristal, J Karjalainen, DR Reed, HJ Westra, MK Evans, D Saleheen, TB Harris, G Dedoussis, G Curhan, M Stumvoll, J Beilby, LR Pasquale, B Feenstra, S Bandinelli, JM Ordovas, AT Chan, U Peters, C Ohlsson, C Gieger, NG Martin, M Waldenberger, DS Siscovick, O Raitakari, JG Eriksson, P Mitchell, DJ Hunter, P Kraft, EB Rimm, DI Boomsma, IB Borecki, RJ Loos, NJ Wareham, P Vollenweider, N Caporaso, HJ Grabe, ML Neuhouser, BH Wolffenbuttel, FB Hu, E Hyppönen, MR Järvelin, LA Cupples, PW Franks, PM Ridker, CM van Duijn, G Heiss, A Metspalu, KE North, E Ingelsson, JA Nettleton, RM van Dam, DI Chasman
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Weight. The EFO term body weight was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
G Thorleifsson, GB Walters, DF Gudbjartsson, V Steinthorsdottir, P Sulem, A Helgadottir, U Styrkarsdottir, S Gretarsdottir, S Thorlacius, I Jonsdottir, T Jonsdottir, EJ Olafsdottir, GH Olafsdottir, T Jonsson, F Jonsson, K Borch-Johnsen, T Hansen, G Andersen, T Jorgensen, T Lauritzen, KK Aben, AL Verbeek, N Roeleveld, E Kampman, LR Yanek, LC Becker, L Tryggvadottir, T Rafnar, DM Becker, J Gulcher, LA Kiemeney, O Pedersen, A Kong, U Thorsteinsdottir, K Stefansson
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Body mass index. The EFO term body mass index was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
G Thorleifsson, GB Walters, DF Gudbjartsson, V Steinthorsdottir, P Sulem, A Helgadottir, U Styrkarsdottir, S Gretarsdottir, S Thorlacius, I Jonsdottir, T Jonsdottir, EJ Olafsdottir, GH Olafsdottir, T Jonsson, F Jonsson, K Borch-Johnsen, T Hansen, G Andersen, T Jorgensen, T Lauritzen, KK Aben, AL Verbeek, N Roeleveld, E Kampman, LR Yanek, LC Becker, L Tryggvadottir, T Rafnar, DM Becker, J Gulcher, LA Kiemeney, O Pedersen, A Kong, U Thorsteinsdottir, K Stefansson
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Smoking behavior. The EFO term smoking behavior was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Gene Ontology (GO) gene set. This set contains genes that have been annotated to the GO term "trans-synaptic signaling by BDNF, modulating synaptic transmission", which is defined as "Cell-cell signaling between presynapse and postsynapse, via the vesicular release and reception of brain derived neurotrophic factor (BDNF), that modulates the synaptic transmission properties of the synapse." 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 "trans-synaptic signaling by BDNF", which is defined as "Cell-cell signaling between presynapse and postsynapse mediated by brain-derived neurotrophic factor (BDNF) crossing the synaptic cleft." 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
Using a two-stage process, several genes were initially identified using microarray analyses of cerebellar tissue from ethanol-treated PKCgamma mutant and wild-type mice. This geneset consists of genes related to PKCgamma wild-type expression changes due to chronic ethanol diet.
Authors:
Bowers BJ, Radcliffe RA, Smith AM, Miyamoto-Ditmon J, Wehner JM
Using a two-stage process, several genes were initially identified using microarray analyses of cerebellar tissue from ethanol-treated PKCgamma mutant and wild-type mice. This geneset consists of genes related to PKCgamma mutant expression changes due to chronic ethanol diet.
Authors:
Bowers BJ, Radcliffe RA, Smith AM, Miyamoto-Ditmon J, Wehner JM
To monitor the expression levels of a large number of genes and to identify genes not previously implicated in traumatic brain injury pathophysiology, a high-density oligonucleotide array containing 8,800 genes was interrogated. RNA samples were prepared from ipsilateral hippocampi 3 hr and 24 hr following lateral cortical impact injury and compared to samples from sham-operated controls.
Authors:
Matzilevich DA, Rall JM, Moore AN, Grill RJ, Dash PK
Study shows that PKC-gamma wild-type mice develop tolerance to the sedative- hypnotic effects of ethanol after chronic ethanol treatment but mutant mice do not, making these genotypes a suitable model for identifying changes in gene expression related developing tolerance toward ethanol. This gene set comprises 27 ethanol- dependence genes that were upregulated in the PKC-gamma wild-type mice during the experiment.
Authors:
Bowers BJ, Radcliffe RA, Smith AM, Miyamoto-Ditmon J, Wehner JM
This gene set comprises 26 ethanol-dependence genes that were upregulated in the PKC-gamma mutant mice during the experiment. Background: Study shows that PKC- gamma wild-type mice develop tolerance to the sedative-hypnotic effects of ethanol after chronic ethanol treatment but mutant mice do not, making these genotypes a suitable model for identifying changes in gene expression related developing tolerance toward ethanol.
Authors:
Bowers BJ, Radcliffe RA, Smith AM, Miyamoto-Ditmon J, Wehner JM
This gene set comprises 17 ethanol-dependence genes that were downregulated in the PKC-gamma mutant mice tested during the experiment. Background: Study shows that PKC-gamma wild-type mice develop tolerance to the sedative-hypnotic effects of ethanol after chronic ethanol treatment but mutant mice do not, making these genotypes a suitable model for identifying changes in gene expression related developing tolerance toward ethanol.
Authors:
Bowers BJ, Radcliffe RA, Smith AM, Miyamoto-Ditmon J, Wehner JM
Acute cocaine - A-FOS mouse vs. Littermate control
Description:
Acute cocaine - A-FOS mouse vs. Littermate control DNA microarray Change in gene expression Animals received a single injection of cocaine (30 mg / kg intraperitoneal) and the striatum harvested at 24 hours. Avadis Microarray analysis software; standard unpaired T-test. A p < 0.001 was used as a cutoff for the selection of genes. Genes are considered up or down regulated if their expression changed 1.4 fold relative to basal conditions. (NIF Table ID 334 [184])
Authors:
Paletzki RF, Myakishev MV, Polesskaya O, Orosz A, Hyman SE, Vinson C
QTL associated with activity response to ethanol 3. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (138125171)
Authors:
Kerns RT, Ravindranathan A, Hassan S, Cage MP, York T, Sikela JM, Williams RW, Miles MF
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