Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-2-18
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1460-9568
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
683-90
pubmed:dateRevised
2010-12-3
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
pubmed:year
2008
pubmed:articleTitle
Genetic background influences the behavioural and molecular consequences of neurokinin-1 receptor knockout.
pubmed:affiliation
Department of Anatomy & Developmental Biology, UCL, Gower St, London, UK. james.mccutcheon@rosalindfranklin.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't