cocaine related behavior 11 (Cocrb11) spans 0 - 27.768945 Mbp (NCBI Build 37) on Chr 11. Obtained from MGI (http://www.informatics.jax.org) by searching for QTLs containing the keyword .
QTL for differences in cocaine responsiveness on Chr11 at D11M!t2 (8.35 Mbp , Build 37)
Description:
differences in cocaine responsiveness spans 0.00 - 33.35 Mbp (NCBI Build 37) on Chr11. 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 Chr11 at Glns-ps1 (18.69 Mbp , Build 37)
Description:
cocaine related behavior spans 0.00 - 43.69 Mbp (NCBI Build 37) on Chr11. 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 chronic alcohol withdrawal severity on Chr11 at D11Mit340 (18.69 Mbp , Build 37)
Description:
chronic alcohol withdrawal severity spans 0.00 - 43.69 Mbp (NCBI Build 37) on Chr11. 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, Kyle Warren R, Crabbe JC, Metten P, Gene Erwin V, Belknap JK
QTL for nicotine sensitivity on Chr11 at D11Mit82 (21.63 Mbp , Build 37)
Description:
nicotine sensitivity spans 0.00 - 46.63 Mbp (NCBI Build 37) on Chr11. This interval was obtained by using an interval width of 25 Mbp around the peak marker (Build 37, MGI, http://informatics.jax.org).
BECs at LORR Recovery Chr# 11 rs3697686(58381052) with right flanking marker rs13480836(5036805) and left marker s3697686(58381052). This was mapped in 300 + (b6x129)F2 mice.
Genes with particular expression in the Anterior olfactory nucleus, dorsal part. Data represent fold expression difference in structure versus grey matter average expression.
Genes with particular expression in the Orbital area, lateral part, layer 1. Data represent fold expression difference in structure versus grey matter average expression.
Alcohol transcriptome changes in mice microglia total homogenate p-value
Description:
Microglia are fundamentally important immune cells within the central nervous system (CNS) that respond to environmental challenges to maintain normal physiological processes. Alterations in steady-state cellular function and over-activation of microglia can facilitate the initiation and progression of neuropathological conditions such as Alzheimer’s disease, Multiple Sclerosis, and Major Depressive Disorder. Alcohol consumption disrupts signaling pathways including both innate and adaptive immune responses that are necessary for CNS homeostasis. Coordinate expression of these genes is not ascertained from an admixture of CNS cell-types, underscoring the importance of examining isolated cellular populations to reveal systematic gene expression changes arising from mature microglia. Unbiased RNA-Seq profiling was used to identify gene expression changes in isolated prefrontal cortical microglia in response to recurring bouts of voluntary alcohol drinking behavior. The voluntary ethanol paradigm utilizes long-term consumption ethanol that results in escalated alcohol intake and altered cortical plasticity that is seen in humans. Gene coexpression analysis identified a coordinately regulated group of genes, unique to microglia, that collectively are associated with alcohol consumption. Genes within this group are involved in toll-like receptor signaling and transforming growth factor beta signaling. Network connectivity of this group identified Siglech as a putative hub gene and highlighted the potential importance of proteases in the microglial response to chronic ethanol. In conclusion, we identified a distinctive microglial gene expression signature for neuroimmune responses related to alcohol consumption that provides valuable insight into microglia-specific changes underlying the development of substance abuse, and possibly other CNS disorders.
Authors:
Gizelle M McCarthy, Sean P Farris, Yuri A Blednov, R Adron Harris, R Dayne Mayfield
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