QTL associated with bone response to mechanical loading 2. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (117360795)
QTL associated with bone response to mechanical loading 3. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (126594840)
Authors:
Kesavan C, Mohan S, Srivastava AK, Kapoor S, Wergedal JE, Yu H, Baylink DJ
QTL associated with wound healing/regeneration 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (105240821)
Authors:
Heber-Katz E, Leferovich JM, Bedelbaeva K, Gourevitch D
QTL associated with heterogeneity in eye lens protein photooxidation kinetics. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (129076217)
Authors:
Wisser KC, Schauerte JA, Burke DT, Galecki A, Chen S, Miller RA, Gafni A
QTL associated with mean platelet volume locus 2. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (105240821)
QTL associated with novelty/stress induced locomotor activation 7. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (119052549)
QTL associated with susceptibility to lung cancer 9. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (118625692)
QTL associated with tibia bone quality traits 2. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (129578831)
Authors:
Jiao Y, Chiu H, Fan Z, Jiao F, Eckstein EC, Beamer WG, Gu W
QTL associated with vertebral morphology and mechanical traits 9. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (129076217)
Authors:
Reeves GM, McCreadie BR, Chen S, Galecki AT, Burke DT, Miller RA, Goldstein SA
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
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.
Authors:
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