Whole Brain Gene Expression Correlates for HOTPLATE_MEANOF2 measured in BXD RI Females obtained using INIA Brain mRNA M430 (Jun06) RMA. The HOTPLATE_MEANOF2 measures Thermal Nociception Hot Plate Avg of 2Trials under the domain Pain. 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
Whole Brain Gene Expression Correlates for HOTPLATE_MEANOF2 measured in BXD RI Females & Males obtained using INIA Brain mRNA M430 (Jun06) RMA. The HOTPLATE_MEANOF2 measures Thermal Nociception Hot Plate Avg of 2Trials under the domain Pain. 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
Whole Brain Gene Expression Correlates for LM_CUE_ACTIVITY measured in BXD RI Males obtained using INIA Brain mRNA M430 (Jun06) RMA. The LM_CUE_ACTIVITY measures Activity in altered context during presentation of cue 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
Whole Brain Gene Expression Correlates for LM_CUE_SUPPRESS measured in BXD RI Males obtained using INIA Brain mRNA M430 (Jun06) RMA. The LM_CUE_SUPPRESS measures Suppression of activity in altered context 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
QTL for ethanol induced locomotion on Chr6 at NA (64.65 Mbp , Build 37)
Description:
ethanol induced locomotion spans 39.65 - 89.65 Mbp (NCBI Build 37) on Chr6. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
Authors:
Hitzemann R, Demarest K, Koyner J, Cipp L, Patel N, Rasmussen E, McCaughran J Jr
QTL for METH responses for home cage activity on Chr6 at D6Nds3 (67.84 Mbp , Build 37)
Description:
METH responses for home cage activity spans 42.84 - 92.84 Mbp (NCBI Build 37) on Chr6. 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 METH responses for body temperature on Chr6 at D6MIt16 (67.84 Mbp , Build 37)
Description:
METH responses for body temperature spans 42.84 - 92.84 Mbp (NCBI Build 37) on Chr6. 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 METH responses for body temperature on Chr6 at D6Nds2 (89.57 Mbp , Build 37)
Description:
METH responses for body temperature spans 64.57 - 114.57 Mbp (NCBI Build 37) on Chr6. 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 high-dose ethanol actions on Chr6 at D6Mit67 (91.93 Mbp , Build 37)
Description:
high-dose ethanol actions spans 66.93 - 116.93 Mbp (NCBI Build 37) on Chr6. 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 differences in cocaine responsiveness on Chr6 at D6Nds2 (93.28 Mbp , Build 37)
Description:
differences in cocaine responsiveness spans 68.28 - 118.28 Mbp (NCBI Build 37) on Chr6. 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 high-dose ethanol actions on Chr6 at D6Mit36 (99.58 Mbp , Build 37)
Description:
high-dose ethanol actions spans 74.58 - 124.58 Mbp (NCBI Build 37) on Chr6. 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 Chr6 at II5ra (101.18 Mbp , Build 37)
Description:
METH responses for home cage activity spans 76.18 - 126.18 Mbp (NCBI Build 37) on Chr6. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
Rotarod Baseline Chr# 6 rs6239023(94005991) with right flanking marker rs13459097(84840296) and left marker rs3718735 (101072507). This was mapped in 300 + (b6x129)F2 mice.
Genes that are induced by THC in CD4 cells in C57BL/6J mice. Gene expression was evaluated via RNA-seq. Values presented are "1" for effect presence. Data taken from Supplemental Data 1.
Authors:
Xiaoming Yang, Marpe Bam, Prakash S Nagarkatti, Mitzi Nagarkatti
Genes identified as expressed lower (down) in the AJ strain than in the S129 strain. Differentially expressed genes had a Q-value < 0.05 following the Benjamini-Hochberg methodology for false discovery rates in the limma+voom pipeline within edgeR. Q-value is reported from the topTable function.
Genes identified as expressed lower (down) in the AJ strain than in the S129 strain. Differentially expressed genes had a Q-value < 0.05 following the Benjamini-Hochberg methodology for false discovery rates in the limma+voom pipeline within edgeR. Q-value is reported from the topTable function.
Genes identified as expressed lower (down) in the AJ strain than in the S129 strain. Differentially expressed genes had a Q-value < 0.05 following the Benjamini-Hochberg methodology for false discovery rates in the limma+voom pipeline within edgeR. Q-value is reported from the topTable function.
Genes identified as expressed lower (down) in the AJ strain than in the S129 strain. Differentially expressed genes had a Q-value < 0.05 following the Benjamini-Hochberg methodology for false discovery rates in the limma+voom pipeline within edgeR. Q-value is reported from the topTable function.
Drug Naïve DO mice were tested for open field, light dark, hole board, novelty place preference before collecting the striatum. RNA-Seq data was analyzed with WGCNA using a soft thresholding power of 3 selected using the WGCNA scale-free topology R2 threshold of 0.9, signed network with a minimum module size of 30, correlation type is bicor, used numeric labels.
Microglia depletion and alcohol gene expression logFC
Description:
Alcohol abuse induces changes in microglia morphology and immune function, but whether microglia initiate or simply amplify the harmful effects of alcohol exposure is still a matter of debate. Here, we determine microglia function in acute and voluntary drinking behaviors using a colony-stimulating factor 1 receptor inhibitor (PLX5622). We show that microglia depletion does not alter the sedative or hypnotic effects of acute intoxication. Microglia depletion also does not change the escalation or maintenance of chronic voluntary alcohol consumption. Transcriptomic analysis revealed that although many immune genes have been implicated in alcohol abuse, down regulation of microglia genes does not necessitate changes in alcohol intake. Instead, microglia depletion and chronic alcohol result in compensatory upregulation of alcohol-responsive, reactive astrocyte genes, indicating astrocytes may play a role in regulation of these alcohol behaviors. Taken together, our behavioral and transcriptional data indicate that microglia are not theprimary effector cell responsible for regulation of acute and voluntary alcohol behaviors. Because microglia depletion did not regulate acute or voluntary alcohol behaviors, we hypothesized that these doses were insufficient to activate microglia and recruit them to an effector phenotype. Therefore, we used a model of repeated immune activation using polyinosinic:polycytidylic acid
Microglia depletion and alcohol gene expression p-value
Description:
Alcohol abuse induces changes in microglia morphology and immune function, but whether microglia initiate or simply amplify the harmful effects of alcohol exposure is still a matter of debate. Here, we determine microglia function in acute and voluntary drinking behaviors using a colony-stimulating factor 1 receptor inhibitor (PLX5622). We show that microglia depletion does not alter the sedative or hypnotic effects of acute intoxication. Microglia depletion also does not change the escalation or maintenance of chronic voluntary alcohol consumption. Transcriptomic analysis revealed that although many immune genes have been implicated in alcohol abuse, down regulation of microglia genes does not necessitate changes in alcohol intake. Instead, microglia depletion and chronic alcohol result in compensatory upregulation of alcohol-responsive, reactive astrocyte genes, indicating astrocytes may play a role in regulation of these alcohol behaviors. Taken together, our behavioral and transcriptional data indicate that microglia are not theprimary effector cell responsible for regulation of acute and voluntary alcohol behaviors. Because microglia depletion did not regulate acute or voluntary alcohol behaviors, we hypothesized that these doses were insufficient to activate microglia and recruit them to an effector phenotype. Therefore, we used a model of repeated immune activation using polyinosinic:polycytidylic acid
We investigated the role of microglia in a mouse model of alcohol dependence using a colony stimulating factor 1 receptor inhibitor (PLX5622) to deplete microglia and a chronic intermittent ethanol vapor two-bottle choice drinking procedure. Additionally, we examined anxiety-like behavior during withdrawal. We then analyzed synaptic neuroadaptations in the central nucleus of the amygdala (CeA) and gene expression changes in the medial prefrontal cortex (mPFC) and CeA from the same animals used for behavioral studies.
Alcohol dependence in the medial prefrontal cortex q-value
Description:
We investigated the role of microglia in a mouse model of alcohol dependence using a colony stimulating factor 1 receptor inhibitor (PLX5622) to deplete microglia and a chronic intermittent ethanol vapor two-bottle choice drinking procedure. Additionally, we examined anxiety-like behavior during withdrawal. We then analyzed synaptic neuroadaptations in the central nucleus of the amygdala (CeA) and gene expression changes in the medial prefrontal cortex (mPFC) and CeA from the same animals used for behavioral studies.
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