Source:http://linkedlifedata.com/resource/pubmed/id/18279320
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2008-2-18
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pubmed:abstractText |
Genetic background affects animal phenotype and therefore is of particular relevance to studies using genetically manipulated mice. Strain differences in hypothalamic-pituitary-adrenocortical (HPA) axis activity may contribute to background-specificity of some mutations. Here, we analysed components of the HPA axis in mice lacking a functional neurokinin-1 receptor (NK1-/-) on two backgrounds: backcrossed C57BL/6 (B6) and mixed C57BL/6 x 129/sv (129B6). We hypothesized that HPA axis activity would vary between these strains, leading to differences in the NK1-/- phenotype. We compared levels of plasma corticosterone between the groups, and found 129B6 mice exhibited elevated levels of stress-induced corticosterone compared with B6 mice, regardless of genotype. Although the level of basal corticotrophin-releasing factor and stress-induced c-fos mRNAs did not differ between the genotypes of either strain, examination of glucocorticoid receptor immunoreactivity within the hippocampus revealed that NK1-/- mice on the 129B6 background had elevated expression compared with wild-type, whilst there was no difference between genotypes in the B6 strain. Similarly, hippocampal neurogenesis in NK1-/- mice was greater than in wild-type on the 129B6 strain, and did not differ between genotypes on the B6 background. Finally, novelty- and morphine-induced locomotion were assessed. NK1-/- mice on the 129B6 background exhibited hyperlocomotion in response to novelty and greater sensitivity to the locomotor-stimulating properties of morphine than wild-type. In contrast, in B6 mice, no differences were observed between genotypes for either locomotor behaviour. In summary, we find that HPA axis activity differs between the strains and that there are profoundly background-specific effects of the NK1 receptor mutation.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Corticosterone,
http://linkedlifedata.com/resource/pubmed/chemical/Morphine,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Glucocorticoid,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Neurokinin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Tachykinins
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1460-9568
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
27
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
683-90
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pubmed:dateRevised |
2010-12-3
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pubmed:meshHeading |
pubmed-meshheading:18279320-Animals,
pubmed-meshheading:18279320-Brain,
pubmed-meshheading:18279320-Cell Proliferation,
pubmed-meshheading:18279320-Corticosterone,
pubmed-meshheading:18279320-Drug Resistance,
pubmed-meshheading:18279320-Exploratory Behavior,
pubmed-meshheading:18279320-Genetic Predisposition to Disease,
pubmed-meshheading:18279320-Genotype,
pubmed-meshheading:18279320-Hippocampus,
pubmed-meshheading:18279320-Hypothalamo-Hypophyseal System,
pubmed-meshheading:18279320-Male,
pubmed-meshheading:18279320-Mice,
pubmed-meshheading:18279320-Mice, Inbred C57BL,
pubmed-meshheading:18279320-Mice, Knockout,
pubmed-meshheading:18279320-Morphine,
pubmed-meshheading:18279320-Motor Activity,
pubmed-meshheading:18279320-Mutation,
pubmed-meshheading:18279320-Phenotype,
pubmed-meshheading:18279320-Receptors, Glucocorticoid,
pubmed-meshheading:18279320-Receptors, Neurokinin-1,
pubmed-meshheading:18279320-Species Specificity,
pubmed-meshheading:18279320-Stress, Physiological,
pubmed-meshheading:18279320-Tachykinins,
pubmed-meshheading:18279320-Up-Regulation
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pubmed:year |
2008
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pubmed:articleTitle |
Genetic background influences the behavioural and molecular consequences of neurokinin-1 receptor knockout.
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pubmed:affiliation |
Department of Anatomy & Developmental Biology, UCL, Gower St, London, UK. james.mccutcheon@rosalindfranklin.edu
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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