Affymetrix oligonucleotide arrays to assess gene expression in brains of mice selectively bred for differences in acute functional tolerance to an incoordinating effect of ethanol (HAFT mice, high acute functional tolerance; LAFT mice, low acute functional tolerance)
This gene set comprises 399 genes that are differentially expressed within each of five brain regions (amygdale, hippocampus, nucleus accumbens, prefrontal cortex and ventral tegmental area) when chronic nicotine treatment is administered to C3H/HeJ mice only. Background: Studies involving use of chronic nicotine treatment identify unique nicotine addiction genes and the biological processes they control in B6 and C3 mice. Results are obtained using gene expression profiling and gene ontology.
Authors:
Wang J, Gutala R, Hwang YY, Kim JM, Konu O, Ma JZ, Li MD
Human neuroblastoma (SH-SY5Y) cells were chronically exposed to nicotine to discover if gene expression was responsible for the long term effects of nicotine on the nervous system and for the up-regulation of acetylcholine receptors upon nicotine exposure. Seventeen genes were found to be differentially expressed. Of these, the genes reported here were down-regulated.
Genes with a mean fold change > 1.5 or < 0.7 were selected and annotated. Values are taken from microarray analysis and represent mean ratios of alcoholic cases compared with matched control cases(n = 6). P values were from t-test; from Flatscher-Bader et al., 2005
Authors:
Flatscher-Bader T, van der Brug M, Hwang JW, Gochee PA, Matsumoto I, Niwa S, Wilce PA
cocaine related behavior 8 (Cocrb8) spans 26.931283 - 76.931283 Mbp (NCBI Build 37) on Chr 9. Obtained from MGI (http://www.informatics.jax.org) by searching for QTLs containing the keyword .
QTL for high-dose ethanol actions on Chr9 at D9Mit42 (21.79 Mbp , Build 37)
Description:
high-dose ethanol actions spans 0.00 - 46.79 Mbp (NCBI Build 37) on Chr9. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
Authors:
Erwin VG, Markel PD, Johnson TE, Gehle VM, Jones BC
QTL for METH responses for home cage activity on Chr9 at Fli-1 (30.20 Mbp , Build 37)
Description:
METH responses for home cage activity spans 5.20 - 55.20 Mbp (NCBI Build 37) on Chr9. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
QTL for morphine antinociception on Chr9 at D9Mit91 (35.00 Mbp , Build 37)
Description:
morphine antinociception spans 10.00 - 60.00 Mbp (NCBI Build 37) on Chr9. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
Authors:
Bergeson SE, Helms ML, O\'Toole LA, Jarvis MW, Hain HS, Mogil JS, Belknap JK
Alcohol preference QTL 1 spans 26931283-76931283 (NCBI Build 37) on Chr9. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org). Phenotypically extreme HAP1/LAP1 animals (n=96) and HAP2/LAP2 animals (n=48) were screened for microsatellite markers in chromosomal regions previously reported to influence alcohol preference phenotypes. Linkage to alcohol preference, Alpq1, mapped to chromosome 9 near D9Mit4 (29 cM) in the HAP1/LAP1 set and near D9Mit90 (9 cM) in the HAP2/LAP2 set. The Alpq1 QTL interval is broad and may contain more than 1 underlying gene. Drd2 at 28 cM is a potential candidate for Alpq1.
Authors:
Bice PJ, Foroud T, Carr LG, Zhang L, Liu L, Grahame NJ, Lumeng L, Li TK, Belknap JK
QTL for cocaine related behavior on Chr9 at D9Mit4 (52.27 Mbp , Build 37)
Description:
cocaine related behavior spans 27.27 - 77.27 Mbp (NCBI Build 37) on Chr9. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
ethanol consumption 3 spans 27.27 - 77.27 Mbp (NCBI Build 37) on Chr9. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
Chronic cocaine - Cocaine-paired (conditioned place preference) vs. Control (saline or cocaine-non-paired) DNA microarray All genes on microarray presented After the pre-conditioning phase where animals were allowed access to either compartment for 15 minutes for 4 consecutive days, the conditioning phase for the cocaine-paired groups and cocaine non-paired groups began, consisting of eight subsequent daily sessions. For both groups, cocaine (10 mg / kg) or saline injections were administered on alternate days. For the cocaine-paired groups, rats were immediately placed in one of the two compartments for 30 min with the door in place restricting a z transformation followed by z test and anova followed by Student-Newman-Keuls' post hoc test. Gene expression profile was assessed 24 h after the last conditioning session that corresponded to 48 h after last cocaine exposure, when drug has been eliminated from the body and transient transcriptional changes are likely to be minimal. Therefore, changes in gene expression at this time-point are likely to reflect longer lasting adaptations that may account for maintenance of cocaine-induced memories. The complete lists of normalized gene expression values for the hippocampus of saline-treated, cocaine non-paired and cocaine-paired groups are presented. Analyses revealed that 214 transcripts were differentially regulated in the hippocampus of cocaine-paired rats vs. non-paired and saline-treated controls. Cocaine-induced conditioned place preference caused significant increases in the expression of 151 genes and caused decreases in the expression of 63 genes. (NIF Table ID 130.1 [83])
Authors:
Krasnova IN, Li SM, Wood WH, McCoy MT, Prabhu VV, Becker KG, Katz JL, Cadet JL
Chronic cocaine - Cocaine-paired (conditioned place preference) vs. Control (saline or cocaine-non-paired) DNA microarray All genes on microarray presented After the pre-conditioning phase where animals were allowed access to either compartment for 15 minutes for 4 consecutive days, the conditioning phase for the cocaine-paired groups and cocaine non-paired groups began, consisting of eight subsequent daily sessions. For both groups, cocaine (10 mg / kg) or saline injections were administered on alternate days. For the cocaine-paired groups, rats were immediately placed in one of the two compartments for 30 min with the door in place restricting a z transformation followed by z test and anova followed by Student-Newman-Keuls' post hoc test. Gene expression profile was assessed 24 h after the last conditioning session that corresponded to 48 h after last cocaine exposure, when drug has been eliminated from the body and transient transcriptional changes are likely to be minimal. Therefore, changes in gene expression at this time-point are likely to reflect longer lasting adaptations that may account for maintenance of cocaine-induced memories. The complete lists of normalized gene expression values for the frontal cortex of saline-treated, cocaine non-paired and cocaine-paired groups are presented. Differences in the expression of 39 transcripts in the frontal cortex were related to the conditioned place preference paradigm. These include increases in the level of 22 genes and decreases in 17 genes. (NIF Table ID 130.3 [83.5])
Authors:
Krasnova IN, Li SM, Wood WH, McCoy MT, Prabhu VV, Becker KG, Katz JL, Cadet JL
Genes associated with Homo sapiens that interact with the MeSH term 'Arsenic' (D001151). Incorporates data from 87 publications curated by the Comparative Toxicogenomics Database (CTD). ODE Gene scores represent number of supporting publications per gene.
Genes associated with Homo sapiens that interact with the MeSH term '5-dihydrocortisone' (C045993). Incorporates data from 1538 publications curated by the Comparative Toxicogenomics Database (CTD). ODE Gene scores represent number of supporting publications per gene.
Genes associated with Homo sapiens that interact with the MeSH term 'Smoke' (D012906). Incorporates data from 54 publications curated by the Comparative Toxicogenomics Database (CTD). ODE Gene scores represent number of supporting publications per gene.
Authors:
None
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