QTL for morphine antinociception on Chr10 at D10Mit51 (19.52 Mbp , Build 37)
Description:
morphine antinociception spans 0.00 - 44.52 Mbp (NCBI Build 37) on Chr10. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
Authors:
Bergeson SE, Helms ML, O\'Toole LA, Jarvis MW, Hain HS, Mogil JS, Belknap JK
QTL for morphine preference on Chr10 at D10MIT282 (24.33 Mbp , Build 37)
Description:
morphine preference spans 0.00 - 49.33 Mbp (NCBI Build 37) on Chr10. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
Authors:
Berrettini WH, Ferraro TN, Alexander RC, Buchberg AM, Vogel WH
QTL associated with amphetamine distance traveled 2. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (20654078)
Authors:
Torkamanzehi A, Boksa P, Ayoubi M, Fortier ME, Ng Ying Kin NM, Skamene E, Rouleau G, Joober R
QTL associated with atherosclerotic lesion area 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (21435099)
QTL associated with atherosclerotic lesion area 2. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (18526522)
QTL associated with experimental allergic encephalomyelitis susceptibility 15. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (21252061)
QTL associated with myeloperoxidase-specific anti-neutrophil cytoplasmic autoantibody QTL 2. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (28871992)
Authors:
Hamano Y, Tsukamoto K, Abe M, Sun GD, Zhang D, Fujii H, Matsuoka S, Tanaka M, Ishida-Okawara A, Tachikawa H, Nishimura H, Tokunaka K, Hirose S, Suzuki K
QTL associated with postnatal body weight growth 9. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (21435099)
QTL associated with proteoglycan induced arthritis 6. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (20654078)
Authors:
Glant TT, Adarichev VA, Nesterovitch AB, Szanto S, Oswald JP, Jacobs JJ, Firneisz G, Zhang J, Finnegan A, Mikecz K
QTL associated with susceptibility to lung cancer 29. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (9133173)
QTL associated with SGC/Knj cross B6 QTL 4. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (28871992)
Authors:
Hamano Y, Tsukamoto K, Abe M, Sun GD, Zhang D, Fujii H, Matsuoka S, Tanaka M, Ishida-Okawara A, Tachikawa H, Nishimura H, Tokunaka K, Hirose S, Suzuki K
QTL associated with voluntary alcohol consumption QTL 6. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (11362694)
The GEO2R tool was used to analyze microarray data from lungs of mice either mock-infected or infected with SARS-CoV1. The Gene sets used in the analysis were from GSE59185. GEO2R was used with default parameters. Genes with an adjusted p-value of <0.05 and a log fold change >1.0 are included in this set. EntrezGene identifiers or sequence identifiers were converted to MGI identifiers. Genes that could not be converted were omitted. If a gene was represented more than once, the largest fold-change was chosen.
Authors:
Jose A Regla-Nava, Jose L Nieto-Torres, Jose M Jimenez-Guardeño, Raul Fernandez-Delgado, Craig Fett, Carlos Castaño-Rodríguez, Stanley Perlman, Luis Enjuanes, Marta L DeDiego
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.
The current study used two inbred mouse strains, C57BL/6 J and A/J, to investigate the genetics of behavioral responses to fentanyl. Mice were tested for conditioned place preference and fentanyl-induced locomotor activity. C57BL/6J mice formed a conditioned place preference to fentanyl injections and fentanyl increased their activity. Neither effect was noted in A/J mice. We conducted RNA-sequencing on the nucleus accumbens of mice used for fentanyl-induced locomotor activity. Surprisingly, we noted few differentially expressed genes using treatment as the main factor. However many genes differed between strains.
Authors:
Samuel J Harp, Mariangela Martini, Will Rosenow, Larry D Mesner, Hugh Johnson, Charles R Farber, Emilie F Rissman
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