QTL for alcohol consumption on Chr1 at D1Mit167 (21.28 Mbp , Build 37)
Description:
alcohol consumption spans 0.00 - 46.28 Mbp (NCBI Build 37) on Chr1. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
Authors:
Vadasz C, Saito M, Gyetvai B, Mikics E, Vadasz C 2nd
QTL for alcohol preference locus on Chr1 at D1Mit295 (22.09 Mbp , Build 37)
Description:
alcohol preference locus spans 0.00 - 47.09 Mbp (NCBI Build 37) on Chr1. 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 alcohol preference locus on Chr1 at D1Mit165 (22.12 Mbp , Build 37)
Description:
alcohol preference locus spans 0.00 - 47.12 Mbp (NCBI Build 37) on Chr1. 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 home cage activity on Chr1 at D1Mit1 (22.85 Mbp , Build 37)
Description:
METH responses for home cage activity spans 0.00 - 47.85 Mbp (NCBI Build 37) on Chr1. 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 morphine antinociception on Chr1 at D1Mit67 (22.97 Mbp , Build 37)
Description:
morphine antinociception spans 0.00 - 47.97 Mbp (NCBI Build 37) on Chr1. 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 associated with "alcohol preference locus 25, male specific". This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (8122863)
QTL associated with amphetamine distance traveled 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (20861477)
Authors:
Torkamanzehi A, Boksa P, Ayoubi M, Fortier ME, Ng Ying Kin NM, Skamene E, Rouleau G, Joober R
QTL associated with collagen induced arthritis 15. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (8122863)
Authors:
Glant TT, Adarichev VA, Nesterovitch AB, Szanto S, Oswald JP, Jacobs JJ, Firneisz G, Zhang J, Finnegan A, Mikecz K
QTL associated with cocaine induced activation 4. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (25567955)
QTL associated with circadian period of locomotor activity 4. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (26691206)
Authors:
Mayeda AR, Hofstetter JR, Belknap JK, Nurnberger JI Jr
QTL associated with lung squamous cell carcinoma 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (24071806)
Authors:
Wang Y, Zhang Z, Yan Y, Lemon WJ, LaRegina M, Morrison C, Lubet R, You M
QTL associated with neurotensin transcript abundance 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (24071806)
QTL associated with systematic lupus erythematosus susceptibility 10. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (19802051)
Authors:
Haywood ME, Hogarth MB, Slingsby JH, Rose SJ, Allen PJ, Thompson EM, Maibaum MA, Chandler P, Davies KA, Simpson E, Walport MJ, Morley BJ
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.
Chronic alcohol abuse alters the molecular structure and function of brain cells. Recent work suggests adaptations made by glial cells, such as astrocytes and microglia, regulate physiological and behavioral changes associated with addiction. Defining how alcohol dependence alters the transcriptome of different cell types is critical for developing the mechanistic hypotheses necessary for a nuanced understanding of cellular signaling in the alcohol-dependent brain. We performed RnA-sequencing on total homogenate and glial cell populations isolated from mouse prefrontal cortex (pfc) following chronic intermittent ethanol vapor exposure (cie). compared with total homogenate, we observed unique and robust gene expression changes in astrocytes and microglia in response to cie. Gene co-expression network analysis revealed biological pathways and hub genes associated with cie in astrocytes and microglia that may regulate alcohol-dependent phenotypes. Astrocyte identity and synaptic calcium signaling genes were enriched in alcohol-associated astrocyte networks, while tGf-β signaling and inflammatory response genes were disrupted by CIE treatment in microglia gene networks. Genes related to innate immune signaling, specifically interferon pathways, were consistently up-regulated across cie-exposed astrocytes, microglia, and total homogenate pfc tissue. This study illuminates the cell-specific effects of chronic alcohol exposure and provides novel molecular targets for studying alcohol dependence.
Authors:
Emma K Erickson, Yuri A Blednov, R Adron Harris, R Dayne Mayfield
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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