Search Criteria: Research Area is "Neurobiology Research: Receptor Defects (dopamine receptor)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 005798 | B6.129P2-Drd5tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 003190 | B6.129S2-Drd2tm1Low/J | Repository-Cryopreserved |
| Mice with a disrupted D2 dopamine receptor gene display chronic hyperprolactinemia and develop anterior lobe lactotrophhyperplasia without evidence of adenomatous transformation. Homozygous mutant mice have no hyperplasia of the intermediate lobe melanotrophs. Aged female D2 receptor homozygous mice develop uterine adenomyosis in response to prolonged prolactin exposure. They also exhibit a locomotor deficit manifested as a 50% reduction in activity and decreased initiation of movement. Female homozygous mice develop prolactinomas of the anterior pituitary gland. Homozygous mice exhibit decreased sensitivity to the rewarding and locomotor effects of ethanol. Drd2tm1Low mice may provide a model for Parkinson's disease. | ||
| 002959 | B6.129S4-Drd1atm1Jcd/J | Repository-Cryopreserved |
| 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 Homozygotes do appear thinner than wildtypes and have a very slight halting gait (unpublished observations, The Jackson Labora
..... For more information please see the full descriiption on the strain data sheet | ||
| 002958 | B6.129S4-Drd3tm1Dac/J | Repository-Cryopreserved |
| Mice homozygous for the Drd3tm1Dac mutation are viable and fertile. They show no gross anatomical or morphological changes. Dopamine antagonist binding studies indicate the absence of D3 receptors in homozygotes and a greatly reduced number in heterozygotes. Behavioral analysis of both homozygous and heterozygous mice reveals hyperactivity, increased locomotor activity and rearing behavior. Behavioral alterations were less pronounced in heterozygotes. D3 receptors are expressed in renal proximal tubules and juxtaglomerular cells and may be responsible for the dopamine-mediated decrease in renin secretion in these cells. Both systolic and diastolic blood pressures were approximately 20 mmHg higher in heterozygotes and homozygotes compared to wild-type mice. | ||
| 007586 | B6;129S4-Drd1atm2Rpa/J | Repository-Cryopreserved |
| 002425 | B6;129S4-Drd3tm1Dac/J | Repository-Cryopreserved |
| Mice homozygous for the Drd3tm1Dac mutation are viable and fertile. They show no gross anatomical or morphological changes. Dopamine antagonist binding studies indicate the absence of D3 receptors in homozygotes and a greatly reduced number in heterozygotes. Behavioral analysis of both homozygous and heterozygous mice reveals hyperactivity, increased locomotor activity and rearing behavior. Behavioral alterations were less pronounced in heterozygotes. D3 receptors are expressed in renal proximal tubules and juxtaglomerular cells and may be responsible for the dopamine-mediated decrease in renin secretion in these cells. Both systolic and diastolic blood pressures were approximately 20 mmHg higher in heterozygotes and homozygotes compared to wild-type mice. | ||
| 002322 | STOCK Drd1atm1Jcd/J | Repository-Cryopreserved |
| 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 Labora
..... For more information please see the full descriiption on the strain data sheet | ||
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Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Under Development
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New Strains Under DevelopmentThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
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- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
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