QTL associated with ethanol induced thermoregulation 3. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (125537552)
QTL associated with vertebral trabecular bone trait 4. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (126237672)
Authors:
Bouxsein ML, Uchiyama T, Rosen CJ, Shultz KL, Donahue LR, Turner CH, Sen S, Churchill GA, Mller R, Beamer WG
QTL associated with "alcohol preference locus 12, male specific". This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (135707912)
QTL associated with "alcohol preference locus 14, female specific". This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (135707912)
QTL associated with postnatal body weight growth 3. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (151943409)
QTL associated with susceptibility to lung cancer 19. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (135707912)
QTL associated with susceptibility to lung cancer 8. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (152030319)
QTL associated with VPA induced neural tube defect. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (129629838)
QTL for alcohol preference locus on Chr7 at D7Mit105 (126.73 Mbp , Build 37)
Description:
alcohol preference locus spans 101.73 - 151.73 Mbp (NCBI Build 37) on Chr7. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
alcohol preference locus 14, female specific at D7Mit105 with a LOD score of 1.84 (p < 0.004) spans and preference correlation of 0.591 101.73 - 151.73 Mbp (NCBI Build 37) on Chr7. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
Here, female High Drinking in the Dark (HDID) mice were stereotaxically injected with 0.5uL rAAV2/5-CMV-Cre-GFP and 0.5uL rAAV2-hSyn-DIO-hM3Dq-mCherry bilaterally into the NAc. A Drinking in the Dark (DID) experiment lasting 6 weeks was carried out with 2 fluid groups (water or ethanol) and 2 treatment groups (VEH/VEH/VEH or VEH/CNO/VEH). Mice were serially treated with vehicle prior to DID during week 1 to establish baseline drinking, CNO (1mg/kg) during weeks 2-5 to measure the effects of chronic treatment, and then mice were treated with vehicle again during week 6 to determine if there were any lasting effects of chronic CNO treatment. This gene set comprises 1,473 genes that were differentially expressed in the nucleus accumbens of ethanol drinking HDID mice treated with vehicle as compared to the water drinking and vehicle treated control group.
Authors:
Darya Y. Pozhidayeva, Sean P. Farris, Calla M. Goeke, Evan J. Firsick, Kayla G. Townsley, Marina Guizzetti, and Angela R. Ozburn
Here, female High Drinking in the Dark (HDID) mice were stereotaxically injected with 0.5uL rAAV2/5-CMV-Cre-GFP and 0.5uL rAAV2-hSyn-DIO-hM3Dq-mCherry bilaterally into the NAc. A Drinking in the Dark (DID) experiment lasting 6 weeks was carried out with 2 fluid groups (water or ethanol) and 2 treatment groups (VEH/VEH/VEH or VEH/CNO/VEH). Mice were serially treated with vehicle prior to DID during week 1 to establish baseline drinking, CNO (1mg/kg) during weeks 2-5 to measure the effects of chronic treatment, and then mice were treated with vehicle again during week 6 to determine if there were any lasting effects of chronic CNO treatment. This gene set comprises 2,377 genes that were differentially expressed in the nucleus accumbens of ethanol drinking HDID mice treated with CNO as compared to the water drinking and vehicle treated control group.
Authors:
Darya Y. Pozhidayeva, Sean P. Farris, Calla M. Goeke, Evan J. Firsick, Kayla G. Townsley, Marina Guizzetti, and Angela R. Ozburn
Gene expression in 212,713 ventral midbrain single nuclei from 95 individuals with history of opioid misuse, and individuals without drug exposure. Chronic exposure to opioids was not associated with change in proportions of glial and neuronal subtypes, however glial transcriptomes were broadly altered, involving 9.5 - 6.2% of expressed genes within microglia, oligodendrocytes, and astrocytes. Genes associated with activation of the immune response including interferon, NFkB signaling, and cell motility pathways were upregulated, contrasting with down-regulated expression of synaptic signaling and plasticity genes in ventral midbrain non-dopaminergic neurons. Ventral midbrain transcriptomic reprogramming in the context of chronic opioid exposure included 325 genes that previous genome-wide studies had linked to risk of substance use traits in the broader population.
Authors:
Julong Wei, Tova Y Lambert, Aditi Valada, Nikhil Patel, Kellie Walker, Jayna Lenders, Carl J Schmidt, Marina Iskhakova, Adnan Alazizi, Henriette Mair-Meijers, Deborah C Mash, Francesca Luca, Roger Pique-Regi, Michael J Bannon, Schahram Akbarian
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