Renthal W, Kumar A, Xiao G, Wilkinson M, Covington HE 3rd, Maze I, Sikder D, Robison AJ, LaPlant Q, Dietz DM, Russo SJ, Vialou V, Chakravarty S, Kodadek TJ, Stack A, Kabbaj M, Nestler EJ
cocaine related behavior 14 (Cocrb14) spans 43.765096 - 93.765096 Mbp (NCBI Build 37) on Chr 15. Obtained from MGI (http://www.informatics.jax.org) by searching for QTLs containing the keyword .
cocaine related behavior 15 (Cocrb15) spans 70.807693 - 120.807693 Mbp (NCBI Build 37) on Chr 15. Obtained from MGI (http://www.informatics.jax.org) by searching for QTLs containing the keyword .
QTL for cocaine related behavior on Chr15 at D15Mit3 (83.88 Mbp , Build 37)
Description:
cocaine related behavior spans 58.88 - 108.88 Mbp (NCBI Build 37) on Chr15. 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 consumption on Chr15 at D15Mit105 (87.33 Mbp , Build 37)
Description:
alcohol consumption spans 62.33 - 112.33 Mbp (NCBI Build 37) on Chr15. 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 cocaine induced activation on Chr15 at NA (92.79 Mbp , Build 37)
Description:
cocaine induced activation spans 67.79 - 117.79 Mbp (NCBI Build 37) on Chr15. 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 Chr15 at D15Mit1 (93.20 Mbp , Build 37)
Description:
METH responses for home cage activity spans 68.20 - 118.20 Mbp (NCBI Build 37) on Chr15. 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 cocaine related behavior on Chr15 at D15Ncvs29 (95.81 Mbp , Build 37)
Description:
cocaine related behavior spans 70.81 - 120.81 Mbp (NCBI Build 37) on Chr15. 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 Chr15 at Spt1 (102.87 Mbp , Build 37)
Description:
METH responses for home cage activity spans 77.87 - 127.87 Mbp (NCBI Build 37) on Chr15. 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 cocaine seizure on Chr15 at D15Mit48 (105.10 Mbp , Build 37)
Description:
cocaine seizure spans 80.10 - 130.10 Mbp (NCBI Build 37) on Chr15. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
Acute and chronic alcohol exposure was analyzed in 534 (C57BL/6J x C3H/HeJ)F2 mice. Behavioral testing was done using 5 traits, acute drug effect, forced ethanol drinking, withdrawal studies ethanol preference and stress induced ethanol drinking. The following QTL were found in a genome wide scan: Following the QTL is the Chromosome , cM location, and LOD score, Eih1 (Chr 1, 85 cM, LOD 6.6), Eih2 (Chr 7, 10 cM, LOD 3.6), Ceih1 (Chr 3, 55 cM, LOD 4.1), Ceih2 (Chr 6, 24.7 cM, LOD 4.1), Ceih3 (Chr 13, 39 cM, LOD 4.1), Eia1(Chr 1, 65 cM, LOD 10.3 and 10.4), Eiwa1 (Chr 7, 50 cM, LOD 4.4), Eiwa2(Chr 11, 43.1 cM, LOD 4.1),Aldd1(Chr 5, 42 cM, LOD 13.2), Aldd2(Chr 12, 18 cM, LOD 5.3),Eiwax1(Chr 1, 79 cM, LOD 6.5), Eiwax2(Chr 5, 59 cM, LOD 15.0), Eiwax3(Chr 12, 21 cM, LOD 3.6), Methp1(Chr 16, 31.4 cM, LOD 4.3), Mec1(Chr 16, 19.4 cM, LOD 5.1), Epbs1(Chr 16, 33 cM, LOD 4.1), Ecbs1(Chr 16, 29.4 cM, LOD 4.8), Mec2(Chr 1, 109 cM, LOD 3.9), Mec3(Chr 2, 109 cM, LOD 4.3), Mec4(Chr 5, 29 cM, LOD 3.9), Mec5(Chr 10, 2 cM, LOD 5.0), Mec6(Chr 15, 49 cM, LOD 5.2, 95% CI 6.7–56.7).
Authors:
Drews E, Rcz I, Lacava AD, Barth A, Bilkei-Gorz A, Wienker TF, Zimmer A
Linkage analysis was performed on a series of Recombinant QTL Introgression (RQI) strains (derived from C57BL/6ByJ and BALB/cJ) to identify QTLs associated with alcohol preference. Male animals from each of 13 RQI strains were tested for 12% alcohol preference and genotyped at 244 polymorphic loci with an average spacing of 6.6 cM. Progenitor strain C57BL/6ByJ exhibits higher alcohol preference than progenitor strain BALB/cJ. Significant linkage to 12% alcohol preference (P<0.0002) mapped to a region of mouse Chromosome 15 spanning markers D15Mit159 (49.6 cM), D15Mit34 (52.2 cM), and D15Mit242 (55.6 cM). The experiment was done in duplicate and the same 3 chromosome 15 markers were detected each time. This locus is named Alprf (alcohol preference.) BALB/cJ-derived alleles confer increased alcohol preference at this locus. Potential candidate genes mapping near Alprf include Ecgf1 (51.6 cM), Cntn1 (55.1 cM), Kif21a (55.1 cM), Pou6f1 (56.6 cM), and Aqp5 (56.8 cM).
Authors:
Vadasz C, Saito M, Balla A, Kiraly I, Vadasz C 2nd, Gyetvai B, Mikics E, Pierson D, Brown D, Nelson JC
Ethanol Preference from BXD lines span 58586243-108586243. This interval was obtained by using an arbitrary interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org). Marker Loci associated with 10% Ethanol Preferences Drinking at p<0.05 (Two Tailed) in the BXD RI set and the Correlation Coefficient, p and Estimated LOD. D15Mit33 (83586243 NCBI 37) p=0.05, LOD=0.08 overall LOD BXD & Select Line 2.4.
QTL for Voluntary Ethanol Consumption on LS x SS RI lines spans 43765164-93765164 .This interval was obtained by using an arbitrary interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org). Chr 15 D15Mit3 39 cM VEC (females) 0.02
In the present study Aaq1, a previously mapped QTL on mouse Chromosome 15 linked to alcohol acceptance, is confirmed using a (C57BL/6J x DBA/2J)F2 population. Aaq1 mapped to 15 cM (D15Mit60)- 48 cM (D15Mit34) on mouse Chromosome 15 with a peak LOD score of 3.8 at approximately 30 cM. C57BL/6J-derived alleles confer increased alcohol acceptance in a dominant fashion at Aaq1. A potential candidate gene for Aaq1 is the peripheral benzodiazepine receptor gene, Bzrp.
Authors:
McClearn GE, Tarantino LM, Rodriguez LA, Jones BC, Blizard DA, Plomin R
QTL mapping results for B6D2F2 mice in regions provisionally identified in BXD RI mice for free-choice ethanol consumption. Peak D15Mit33 58586243-108586243. This interval was obtained by using an arbitrary interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org)
H3K4me3 promoters of NPC of 129SvJae x C57BL/6 mice. This is Chromatin IP against H3K4me3 and 1 binary 1 value for identified.
Authors:
Mikkelsen TS, Ku M, Jaffe DB, Issac B, Lieberman E, Giannoukos G, Alvarez P, Brockman W, Kim TK, Koche RP, Lee W, Mendenhall E, O\'Donovan A, Presser A, Russ C, Xie X, Meissner A, Wernig M, Jaenisch R, Nusbaum C, Lander ES, Bernstein BE
chromatin immunoprecipitation coupled with promoter microarray analysis to characterize genome-wide H3 acetylation increases in the mouse nucleus accumbens after repeated cocaine administration.
Transcriptomic analysis of gene expression in the nucleus accumbens somatostatin interneurons of male 8�12-week-old Sst-Cre mice or Sst-Cre x TLG498 (SST-TLG498) mice following repeated cocaine intake. Expression was measured via RNA-seq. Values presented are p-values. Data taken from Supplementary Data 1. Data can be accessed at GEO with accession number: GSE116484.A7
Authors:
Efrain A Ribeiro, Marine Salery, Joseph R Scarpa, Erin S Calipari, Peter J Hamilton, Stacy M Ku, Hope Kronman, Immanuel Purushothaman, Barbara Juarez, Mitra Heshmati, Marie Doyle, Casey Lardner, Dominicka Burek, Ana Strat, Stephen Pirpinias, Ezekiell Mouzon, Ming-Hu Han, Rachael L Neve, Rosemary C Bagot, Andrew Kasarskis, Ja Wook Koo, Eric J Nestler
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
Microglia depletion and alcohol gene expression p-value
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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