These Drd1 knock-out mice exhibit growth retardation and behavioral anomalies. They are suitable for use in applications related to the study of the interaction of dopamine receptors and neuronal pathways.
IMR Colony, The Jackson Laboratory
Genetic Background | Generation |
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000664 C57BL/6J |
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Allele Type | Gene Symbol | Gene Name |
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Targeted (Null/Knockout) | Drd1 | dopamine receptor D1 |
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 Homozygotes do appear thinner than wildtypes and have a very slight halting gait (unpublished observations, The Jackson Laboratory).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. J1 ES cells were used.
Allele Name | targeted mutation 1, John Drago |
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Allele Type | Targeted (Null/Knockout) |
Allele Synonym(s) | D1-; D1A-; D1r- |
Gene Symbol and Name | Drd1, dopamine receptor D1 |
Gene Synonym(s) | |
Strain of Origin | 129S4/SvJae |
Chromosome | 13 |
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 heterozygous matings. Homozygotes are smaller than normal littermates and have a scruffy appearing coat. Homozygous mutants are usually not healthy enough ship. Expected coat color from breeding:Black
When using the D1A- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002959 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
---|---|---|
Heterozygous or wildtype for Drd1a<tm1Jcd> |
Frozen Mouse Embryo | B6.129S4-Drd1<tm1Jcd>/J Frozen Embryos | $2595.00 |
Frozen Mouse Embryo | B6.129S4-Drd1<tm1Jcd>/J Frozen Embryos | $2595.00 |
Frozen Mouse Embryo | B6.129S4-Drd1<tm1Jcd>/J Frozen Embryos | $3373.50 |
Frozen Mouse Embryo | B6.129S4-Drd1<tm1Jcd>/J Frozen Embryos | $3373.50 |
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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