Immune protein expression change in rat NAc after low fentanyl intake abstinence vs. control_FC
Description:
Male, Sprague-Dawley rats (n = 17); Envigo, Indianapolis, IN) weighing between 250 and 300 g at the start of experiments were used. Rats were trained to lever press for fentanyl (0.0032 mg/kg/0.1 mL infusion) or saline (0.1 mL/inf) using established methods (Neelakantan et al., 2017). Two rats were excluded due to loss of catheter patency. Twenty-four hours following the final self-administration session, rats were sacrificed for molecular biology analyses (n = 15). Due to individual differences and variability in the levels of opioid intake, animals sacrificed for molecular analyses were stratified according to lifetime fentanyl intake: 0 mg/kg fentanyl [i.e., saline self-administration rats (n = 5)], <1.2 mg/kg fentanyl [“low” self-administration rats (n = 5)] and >1.2 mg/kg fentanyl [“high” self-administration rats (n = 5)]. Protein homogenates from the NAc, CPu, and HIP were assayed by a BioPlex immunoassay panel that includes granulocyte–macrophage colony stimulating factor (GMCSF), granulocyte-colony stimulating factor (GCSF), interferon gamma (IFNγ), IL1 β, monocyte chemoattractant protein 1 (MCP1), interleukin (IL)2, IL4, IL5, IL7, IL10, IL12 active heterodimer (IL12p70), IL17A, IL18, macrophage inflammatory protein 3 (MIP3 α), chemokine ligand 5 (RANTES) and tumor necrosis factor alpha (TNF α) (see Heat Map).
Authors:
Chiomah Ezeomah, Kathryn A Cunningham, Sonja J Stutz, Robert G Fox, Natalya Bukreyeva, Kelly T Dineley, Slobodan Paessler, Irma E Cisneros
Immune protein expression change in rat Nac after high fentanyl intake abstinence vs. control_FC
Description:
Male, Sprague-Dawley rats (n = 17); Envigo, Indianapolis, IN) weighing between 250 and 300 g at the start of experiments were used. Rats were trained to lever press for fentanyl (0.0032 mg/kg/0.1 mL infusion) or saline (0.1 mL/inf) using established methods (Neelakantan et al., 2017). Two rats were excluded due to loss of catheter patency. Twenty-four hours following the final self-administration session, rats were sacrificed for molecular biology analyses (n = 15). Due to individual differences and variability in the levels of opioid intake, animals sacrificed for molecular analyses were stratified according to lifetime fentanyl intake: 0 mg/kg fentanyl [i.e., saline self-administration rats (n = 5)], <1.2 mg/kg fentanyl [“low” self-administration rats (n = 5)] and >1.2 mg/kg fentanyl [“high” self-administration rats (n = 5)]. Protein homogenates from the NAc, CPu, and HIP were assayed by a BioPlex immunoassay panel that includes granulocyte–macrophage colony stimulating factor (GMCSF), granulocyte-colony stimulating factor (GCSF), interferon gamma (IFNγ), IL1 β, monocyte chemoattractant protein 1 (MCP1), interleukin (IL)2, IL4, IL5, IL7, IL10, IL12 active heterodimer (IL12p70), IL17A, IL18, macrophage inflammatory protein 3 (MIP3 α), chemokine ligand 5 (RANTES) and tumor necrosis factor alpha (TNF α) (see Heat Map).
Authors:
Chiomah Ezeomah, Kathryn A Cunningham, Sonja J Stutz, Robert G Fox, Natalya Bukreyeva, Kelly T Dineley, Slobodan Paessler, Irma E Cisneros
Immune protein expression change in rat CPu after low fentanyl intake abstinence vs. control_FC
Description:
Male, Sprague-Dawley rats (n = 17); Envigo, Indianapolis, IN) weighing between 250 and 300 g at the start of experiments were used. Rats were trained to lever press for fentanyl (0.0032 mg/kg/0.1 mL infusion) or saline (0.1 mL/inf) using established methods (Neelakantan et al., 2017). Two rats were excluded due to loss of catheter patency. Twenty-four hours following the final self-administration session, rats were sacrificed for molecular biology analyses (n = 15). Due to individual differences and variability in the levels of opioid intake, animals sacrificed for molecular analyses were stratified according to lifetime fentanyl intake: 0 mg/kg fentanyl [i.e., saline self-administration rats (n = 5)], <1.2 mg/kg fentanyl [“low” self-administration rats (n = 5)] and >1.2 mg/kg fentanyl [“high” self-administration rats (n = 5)]. Protein homogenates from the NAc, CPu, and HIP were assayed by a BioPlex immunoassay panel that includes granulocyte–macrophage colony stimulating factor (GMCSF), granulocyte-colony stimulating factor (GCSF), interferon gamma (IFNγ), IL1 β, monocyte chemoattractant protein 1 (MCP1), interleukin (IL)2, IL4, IL5, IL7, IL10, IL12 active heterodimer (IL12p70), IL17A, IL18, macrophage inflammatory protein 3 (MIP3 α), chemokine ligand 5 (RANTES) and tumor necrosis factor alpha (TNF α) (see Heat Map).
Authors:
Chiomah Ezeomah, Kathryn A Cunningham, Sonja J Stutz, Robert G Fox, Natalya Bukreyeva, Kelly T Dineley, Slobodan Paessler, Irma E Cisneros
Immune protein expression change in rat CPu after high fentanyl intake abstinence vs. control_FC
Description:
Male, Sprague-Dawley rats (n = 17); Envigo, Indianapolis, IN) weighing between 250 and 300 g at the start of experiments were used. Rats were trained to lever press for fentanyl (0.0032 mg/kg/0.1 mL infusion) or saline (0.1 mL/inf) using established methods (Neelakantan et al., 2017). Two rats were excluded due to loss of catheter patency. Twenty-four hours following the final self-administration session, rats were sacrificed for molecular biology analyses (n = 15). Due to individual differences and variability in the levels of opioid intake, animals sacrificed for molecular analyses were stratified according to lifetime fentanyl intake: 0 mg/kg fentanyl [i.e., saline self-administration rats (n = 5)], <1.2 mg/kg fentanyl [“low” self-administration rats (n = 5)] and >1.2 mg/kg fentanyl [“high” self-administration rats (n = 5)]. Protein homogenates from the NAc, CPu, and HIP were assayed by a BioPlex immunoassay panel that includes granulocyte–macrophage colony stimulating factor (GMCSF), granulocyte-colony stimulating factor (GCSF), interferon gamma (IFNγ), IL1 β, monocyte chemoattractant protein 1 (MCP1), interleukin (IL)2, IL4, IL5, IL7, IL10, IL12 active heterodimer (IL12p70), IL17A, IL18, macrophage inflammatory protein 3 (MIP3 α), chemokine ligand 5 (RANTES) and tumor necrosis factor alpha (TNF α) (see Heat Map).
Authors:
Chiomah Ezeomah, Kathryn A Cunningham, Sonja J Stutz, Robert G Fox, Natalya Bukreyeva, Kelly T Dineley, Slobodan Paessler, Irma E Cisneros
Immune protein expression change in rat HIP after low fentanyl intake abstinence vs. control_FC
Description:
Male, Sprague-Dawley rats (n = 17); Envigo, Indianapolis, IN) weighing between 250 and 300 g at the start of experiments were used. Rats were trained to lever press for fentanyl (0.0032 mg/kg/0.1 mL infusion) or saline (0.1 mL/inf) using established methods (Neelakantan et al., 2017). Two rats were excluded due to loss of catheter patency. Twenty-four hours following the final self-administration session, rats were sacrificed for molecular biology analyses (n = 15). Due to individual differences and variability in the levels of opioid intake, animals sacrificed for molecular analyses were stratified according to lifetime fentanyl intake: 0 mg/kg fentanyl [i.e., saline self-administration rats (n = 5)], <1.2 mg/kg fentanyl [“low” self-administration rats (n = 5)] and >1.2 mg/kg fentanyl [“high” self-administration rats (n = 5)]. Protein homogenates from the NAc, CPu, and HIP were assayed by a BioPlex immunoassay panel that includes granulocyte–macrophage colony stimulating factor (GMCSF), granulocyte-colony stimulating factor (GCSF), interferon gamma (IFNγ), IL1 β, monocyte chemoattractant protein 1 (MCP1), interleukin (IL)2, IL4, IL5, IL7, IL10, IL12 active heterodimer (IL12p70), IL17A, IL18, macrophage inflammatory protein 3 (MIP3 α), chemokine ligand 5 (RANTES) and tumor necrosis factor alpha (TNF α) (see Heat Map).
Authors:
Chiomah Ezeomah, Kathryn A Cunningham, Sonja J Stutz, Robert G Fox, Natalya Bukreyeva, Kelly T Dineley, Slobodan Paessler, Irma E Cisneros
Immune protein expression change in rat HIP after high fentanyl intake abstinence vs. control_FC
Description:
Male, Sprague-Dawley rats (n = 17); Envigo, Indianapolis, IN) weighing between 250 and 300 g at the start of experiments were used. Rats were trained to lever press for fentanyl (0.0032 mg/kg/0.1 mL infusion) or saline (0.1 mL/inf) using established methods (Neelakantan et al., 2017). Two rats were excluded due to loss of catheter patency. Twenty-four hours following the final self-administration session, rats were sacrificed for molecular biology analyses (n = 15). Due to individual differences and variability in the levels of opioid intake, animals sacrificed for molecular analyses were stratified according to lifetime fentanyl intake: 0 mg/kg fentanyl [i.e., saline self-administration rats (n = 5)], <1.2 mg/kg fentanyl [“low” self-administration rats (n = 5)] and >1.2 mg/kg fentanyl [“high” self-administration rats (n = 5)]. Protein homogenates from the NAc, CPu, and HIP were assayed by a BioPlex immunoassay panel that includes granulocyte–macrophage colony stimulating factor (GMCSF), granulocyte-colony stimulating factor (GCSF), interferon gamma (IFNγ), IL1 β, monocyte chemoattractant protein 1 (MCP1), interleukin (IL)2, IL4, IL5, IL7, IL10, IL12 active heterodimer (IL12p70), IL17A, IL18, macrophage inflammatory protein 3 (MIP3 α), chemokine ligand 5 (RANTES) and tumor necrosis factor alpha (TNF α) (see Heat Map).
Authors:
Chiomah Ezeomah, Kathryn A Cunningham, Sonja J Stutz, Robert G Fox, Natalya Bukreyeva, Kelly T Dineley, Slobodan Paessler, Irma E Cisneros
GSE32423_MEMORY_VS_NAIVE_CD8_TCELL_IL7_IL4_UP
Genes up-regulated in comparison of memory CD8 T cells treated with IL4 <a href='http://www.ncbi.nlm.nih.gov/gene/3565'>[GeneID=3565]</a> and IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a> versus naive CD8 T cells treated with IL4 <a href='http://www.ncbi.nlm.nih.gov/gene/3565'>[GeneID=3565]</a> and IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a>.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE32423_IL7_VS_IL7_IL4_NAIVE_CD8_TCELL_DN
Genes down-regulated in comparison of naive CD8 T cells treated with IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a> versus those treated with IL4 <a href='http://www.ncbi.nlm.nih.gov/gene/3565'>[GeneID=3565]</a> and IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a>.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE32423_IL7_VS_IL7_IL4_MEMORY_CD8_TCELL_DN
Genes down-regulated in comparison of memory CD8 T cells treated with IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a> versus those treated with IL4 <a href='http://www.ncbi.nlm.nih.gov/gene/3565'>[GeneID=3565]</a> and IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a>.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE32423_IL7_VS_IL7_IL4_MEMORY_CD8_TCELL_UP
Genes up-regulated in comparison of memory CD8 T cells treated with IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a> versus those treated with IL4 <a href='http://www.ncbi.nlm.nih.gov/gene/3565'>[GeneID=3565]</a> and IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a>.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE32423_MEMORY_VS_NAIVE_CD8_TCELL_IL7_DN
Genes down-regulated in comparison of memory CD8 T cells treated with IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a> versus naive CD8 T cells treated with IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a>.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE32423_MEMORY_VS_NAIVE_CD8_TCELL_IL7_IL4_DN
Genes down-regulated in comparison of memory CD8 T cells treated with IL4 <a href='http://www.ncbi.nlm.nih.gov/gene/3565'>[GeneID=3565]</a> and IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a> versus naive CD8 T cells treated with IL4 <a href='http://www.ncbi.nlm.nih.gov/gene/3565'>[GeneID=3565]</a> and IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a>.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE32423_IL7_VS_IL7_IL4_NAIVE_CD8_TCELL_UP
Genes up-regulated in comparison of naive CD8 T cells treated with IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a> versus those treated with IL4 <a href='http://www.ncbi.nlm.nih.gov/gene/3565'>[GeneID=3565]</a> and IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a>.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
GSE32423_MEMORY_VS_NAIVE_CD8_TCELL_IL7_UP
Genes up-regulated in comparison of memory CD8 T cells treated with IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a> versus naive CD8 T cells treated with IL7 <a href='http://www.ncbi.nlm.nih.gov/gene/3574'>[GeneID=3574]</a>.
c7 - Genesets containing immunologic signatures defined directly from microarray gene expression data from immunologic studies.
Molecular Signatures Database (MSigDB) Geneset. This geneset was imported from one of the MSigDB collections.
gene2msig v. 0.1.0
Last updated 2015.08.31
Cerebellum Gene Expression Correlates for LM_SUPPRESSION measured in BXD RI Males obtained using SJUT Cerebellum mRNA M430 (Mar05) RMA. The LM_SUPPRESSION measures Cue Conditioning - Activity suppression after 3rd tone/shock pairing under the domain Basal Behavior. The correlates were thresholded at a p-value of less than 0.001.
Authors:
Philip VM, Duvvuru S, Gomero B, Ansah TA, Blaha CD, Cook MN, Hamre KM, Lariviere WR, Matthews DB, Mittleman G, Goldowitz D, Chesler EJ
Striatum Gene Expression Correlates for COCA_BASE_DRUG measured in BXD RI Males obtained using GeneNetwork Striatum M430V2 (Apr05) RMA. The COCA_BASE_DRUG measures CPP - Time (s) in drug-paired compartment a under the domain Cocaine. The correlates were thresholded at a p-value of less than 0.001.
Authors:
Philip VM, Duvvuru S, Gomero B, Ansah TA, Blaha CD, Cook MN, Hamre KM, Lariviere WR, Matthews DB, Mittleman G, Goldowitz D, Chesler EJ
Striatum Gene Expression Correlates for COCA_TIME_BASELINE measured in BXD RI Males obtained using GeneNetwork Striatum M430V2 (Apr05) RMA. The COCA_TIME_BASELINE measures Cocaine CPP - Proportion of time spent in conditioned side prior to conditioning under the domain Cocaine. The correlates were thresholded at a p-value of less than 0.001.
Authors:
Philip VM, Duvvuru S, Gomero B, Ansah TA, Blaha CD, Cook MN, Hamre KM, Lariviere WR, Matthews DB, Mittleman G, Goldowitz D, Chesler EJ
Cerebellum Gene Expression Correlates for MDMA_ACT_SAL_2 measured in BXD RI Females obtained using SJUT Cerebellum mRNA M430 (Mar05) RMA. The MDMA_ACT_SAL_2 measures Locomotor activity after second saline treatment. under the domain MDMA. The correlates were thresholded at a p-value of less than 0.001.
Authors:
Philip VM, Duvvuru S, Gomero B, Ansah TA, Blaha CD, Cook MN, Hamre KM, Lariviere WR, Matthews DB, Mittleman G, Goldowitz D, Chesler EJ
QTL for METH responses for home cage activity on Chr3 at Evi1 (30.85 Mbp , Build 37)
Description:
METH responses for home cage activity spans 5.85 - 55.85 Mbp (NCBI Build 37) on Chr3. 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.
GeneWeaver