QTL for ethanol withdrawal on Chr12 at D12Ncvs38 (14.25 Mbp , Build 37)
Description:
ethanol withdrawal spans 0.00 - 39.25 Mbp (NCBI Build 37) on Chr12. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
Ethanol induced LORR Chr# 12 rs6344105 (68860209) with right flanking marker rs3661760 (59053677) and left marker rs13481604(99317323). This was mapped in 300 + (b6x129)F2 mice.
Average rotarod training latency Chr# 12 rs13481614 (102385663) with right flanking marker rs33846822 (30605487) and left marker rs29187760 (115166913). This was mapped in 300 + (b6x129)F2 mice.
QTL associated with "alcohol acceptance QTL 2, female specific". This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (61756236)
QTL associated with atherosclerotic lesion area 6. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (55072816)
QTL associated with cytokine deficiency colitis susceptibility 7. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (82743296)
Authors:
Mhler M, Most C, Schmidtke S, Sundberg JP, Li R, Hedrich HJ, Churchill GA
QTL associated with cytokine deficiency colitis susceptibility 8. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (82743296)
Authors:
Mhler M, Most C, Schmidtke S, Sundberg JP, Li R, Hedrich HJ, Churchill GA
QTL associated with Crhr1 transcript abundance QTL 2. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (82010921)
QTL associated with directional asymmetry QTL 7. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (72355580)
QTL associated with hereditary spherocytosis modifer 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (80557940)
Authors:
Peters LL, Swearingen RA, Andersen SG, Gwynn B, Lambert AJ, Li R, Lux SE, Churchill GA
QTL associated with pulmonary adenoma resistance 3. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (82010921)
Authors:
Pearson HB, Perez-Mancera PA, Dow LE, Ryan A, Tennstedt P, Bogani D, Elsum I, Greenfield A, Tuveson DA, Simon R, Humbert PO
QTL associated with postnatal body weight growth 12. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (80094377)
QTL associated with vertebral trabecular bone trait 13. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (71186215)
Authors:
Bouxsein ML, Uchiyama T, Rosen CJ, Shultz KL, Donahue LR, Turner CH, Sen S, Churchill GA, Mller R, Beamer WG
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
Authors:
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