These Drd1 knock-out mice exhibit mutation exhibit growth retardation, down-regulated expression of dynorphin and substance P, along with behavioral anomalies. They are suitable for use in applications related to the study of dopamine receptors.
Dr. Heiner Westphal, National Institutes of Health
Mice homozygous for the Drd1atm1Jcd targeted mutation exhibit growth retardation and show down-regulated expression of dynorphin and substance P. They also show behavioral anomolies in spatial learning, movement initiation, and responses to new stimuli. Administration of cocaine to homozygotes does not activate locomotion or up-regulate immediate early gene (IEG) expression; however, dopamine receptor-2-dependent IEG changes are intact. Acute cocaine administration increases substance P levels. Failure of locomotor activation is also seen with repeated amphetamine treatment. Dopamine receptor D1a deficient mice do retain cocaine-conditioned place preference. Please Note: Growth retardation, which may be due to abnormal or delayed tooth formation, is avoided if homozygotes are fed either hydrated or crushed grain from ~2-10 weeks of age. Homozygotes do appear thinner than wildtypes and have a very slight halting gait (unpublished observations, The Jackson Laboratory). Heterozygous mice are unaffected.
This targeted mutant was made by Dr. John Drago in the laboratory of Dr. Heiner Westphal of the National Institute of Child Health and Human Development. A targeting vector was used which resulted in the neomycin-resistant gene (neo) replacing all coding sequences of the Drd1 gene. 129S4/SvJae-derived J1 ES cells were used. The strain was maintained on a mixed B6;129 background, and may contain FVB.
|Allele Name||targeted mutation 1, John Drago|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||D1-; D1A-; D1r-|
|Gene Symbol and Name||Drd1, dopamine receptor D1|
|Strain of Origin||129S4/SvJae|
|Molecular Note||A neomycin resistance cassette replaced 0.75kb of sequence encoding the fifth transmembrane domain and third intracytoplasmic loop.|
|Mutations Made By|| |
Dr. John Drago, National Institutes of Health
This strain is maintained by mating homozygous siblings.
When using the D1A- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002322 in your Materials and Methods section.