Strain Name:

B6.129S2-Drd2tm1Low/J

Stock Number:

003190

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Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain C57BL/6
Donor Strain 129S2 via D3 ES cell line
 
Donating InvestigatorDr. Malcolm J Low,   University of Michigan Medical School

Description
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.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

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Parkinson's Disease Models
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017001   129S.B6N-Plk2tm1Elan/J
016198   129S6.Cg-Tg(Camk2a-tTA)1Mmay/JlwsJ
004608   B6(Cg)-Htra2mnd2/J
021828   B6(SJL)-Lrrk2tm3.1Mjff/J
008133   B6.129-Sncbtm1Sud/J
008084   B6.129P2-Drd4tm1Dkg/J
004744   B6.129P2-Esr1tm1Ksk/J
013586   B6.129P2-Gt(ROSA)26Sortm1Nik/J
002609   B6.129P2-Nos2tm1Lau/J
008843   B6.129P2-Sncgtm1Vlb/J
016566   B6.129S-Hcn1tm2Kndl/J
004322   B6.129S1-Mapk10tm1Flv/J
006582   B6.129S4-Park2tm1Shn/J
017946   B6.129S4-Pink1tm1Shn/J
005934   B6.129S4-Ucp2tm1Lowl/J
004936   B6.129S6(Cg)-Spp1tm1Blh/J
012453   B6.129X1(FVB)-Lrrk2tm1.1Cai/J
017009   B6.129X1-Nfe2l2tm1Ywk/J
009346   B6.Cg-Lrrk2tm1.1Shn/J
005491   B6.Cg-Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
006577   B6.Cg-Park7tm1Shn/J
000567   B6.Cg-T2J +/+ Qkqk-v/J
007004   B6.Cg-Tg(Camk2a-tTA)1Mmay/DboJ
003139   B6.Cg-Tg(DBHn-lacZ)8Rpk/J
007673   B6.Cg-Tg(Gad1-EGFP)3Gfng/J
012466   B6.Cg-Tg(Lrrk2)6Yue/J
012467   B6.Cg-Tg(Lrrk2*G2019S)2Yue/J
008323   B6.Cg-Tg(Mc4r-MAPT/Sapphire)21Rck/J
008321   B6.Cg-Tg(Npy-MAPT/Sapphire)1Rck/J
008324   B6.Cg-Tg(Pmch-MAPT/CFP)1Rck/J
008322   B6.Cg-Tg(Pomc-MAPT/Topaz)1Rck/J
007894   B6.Cg-Tg(Rgs4-EGFP)4Lvt/J
012588   B6.Cg-Tg(TH-ALPP)1Erav/J
012265   B6.Cg-Tg(THY1-SNCA*A30P)TS2Sud/J
008859   B6.Cg-Tg(THY1-SNCA*A53T)F53Sud/J
008135   B6.Cg-Tg(THY1-SNCA*A53T)M53Sud/J
008601   B6.Cg-Tg(Th-cre)1Tmd/J
013583   B6.Cg-Tg(tetO-LRRK2)C7874Cai/J
000544   B6.D2-Cacna1atg/J
012445   B6.FVB-Tg(LRRK2)WT1Mjfa/J
012446   B6.FVB-Tg(LRRK2*G2019S)1Mjfa/J
006660   B6.SJL-Slc6a3tm1.1(cre)Bkmn/J
008364   B6;129-Chattm1(cre/ERT)Nat/J
009688   B6;129-Dbhtm2(Th)Rpa Thtm1Rpa/J
008883   B6;129-Gt(ROSA)26Sortm1(SNCA*A53T)Djmo/TmdJ
008889   B6;129-Gt(ROSA)26Sortm2(SNCA*119)Djmo/TmdJ
008886   B6;129-Gt(ROSA)26Sortm3(SNCA*E46K)Djmo/TmdJ
009347   B6;129-Lrrk2tm1.1Shn/J
016209   B6;129-Lrrk2tm2.1Shn/J
016210   B6;129-Lrrk2tm3.1Shn/J
013050   B6;129-Pink1tm1Aub/J
004807   B6;129-Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa/Mmjax
006390   B6;129-Sncatm1Sud Sncbtm1.1Sud/J
008532   B6;129-Thtm1(cre/Esr1)Nat/J
008333   B6;129P2-Dldtm1Ptl/J
008333   B6;129P2-Dldtm1Ptl/J
002596   B6;129P2-Nos2tm1Lau/J
003243   B6;129S-Tnfrsf1atm1Imx Tnfrsf1btm1Imx/J
003692   B6;129X1-Sncatm1Rosl/J
016575   B6;C3-Tg(PDGFB-LRRK2*G2019S)340Djmo/J
016576   B6;C3-Tg(PDGFB-LRRK2*R1441C)574Djmo/J
008169   B6;C3-Tg(Prnp-MAPT*P301S)PS19Vle/J
004479   B6;C3-Tg(Prnp-SNCA*A53T)83Vle/J
000231   B6;C3Fe a/a-Csf1op/J
012450   B6;D2-Tg(tetO-SNCA)1Cai/J
013725   B6;SJL-Tg(LRRK2)66Mjff/J
008473   B6;SJL-Tg(THY1-SNCA*A30P)M30Sud/J
008134   B6;SJL-Tg(THY1-SNCA*A30P)TS2Sud/J
016976   B6C3-Tg(tetO-SNCA*A53T)33Vle/J
000506   B6C3Fe a/a-Qkqk-v/J
003741   B6D2-Tg(Prnp-MAPT)43Vle/J
024841   B6N.Cg-Tg(Prnp-MAPT*P301S)PS19Vle/J
018768   B6N.Cg-Tg(SNCA*E46K)3Elan/J
012621   C.129S(B6)-Chrna3tm1.1Hwrt/J
016120   C57BL/6-Lrrk1tm1.1Mjff/J
012444   C57BL/6-Lrrk2tm1Mjfa/J
008389   C57BL/6-Tg(THY1-SNCA)1Sud/J
012769   C57BL/6-Tg(Thy1-Sncg)HvP36Putt/J
005706   C57BL/6-Tg(tetO-CDK5R1/GFP)337Lht/J
006618   C57BL/6-Tg(tetO-COX8A/EYFP)1Ksn/J
018785   C57BL/6J-Tg(LRRK2*G2019S)2AMjff/J
018786   C57BL/6J-Tg(LRRK2*R1441G)3IMjff/J
008245   C57BL/6J-Tg(Th-SNCA)5Eric/J
008239   C57BL/6J-Tg(Th-SNCA*A30P*A53T)39Eric/J
016122   C57BL/6N-Lrrk1tm1.1Mjff Lrrk2tm1.1Mjff/J
016121   C57BL/6N-Lrrk2tm1.1Mjff/J
016123   C57BL/6N-Sncatm1Mjff/J
016936   C57BL/6N-Tg(Thy1-SNCA)12Mjff/J
017682   C57BL/6N-Tg(Thy1-SNCA)15Mjff/J
007677   CB6-Tg(Gad1-EGFP)G42Zjh/J
009610   FVB/N-Tg(LRRK2)1Cjli/J
009609   FVB/N-Tg(LRRK2*G2019S)1Cjli/J
009604   FVB/N-Tg(LRRK2*R1441G)135Cjli/J
009090   FVB/NJ-Tg(Slc6a3-PARK2*Q311X)AXwy/J
017678   FVB;129-Pink1tm1Aub Tg(Prnp-SNCA*A53T)AAub/J
017744   FVB;129-Tg(Prnp-SNCA*A53T)AAub/J
010710   FVB;129S6-Sncatm1Nbm Tg(SNCA)1Nbm/J
010788   FVB;129S6-Sncatm1Nbm Tg(SNCA*A30P)1Nbm Tg(SNCA*A30P)2Nbm/J
010799   FVB;129S6-Sncatm1Nbm Tg(SNCA*A53T)1Nbm Tg(SNCA*A53T)2Nbm/J
004808   STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
000942   STOCK Pitx3ak/2J
014092   STOCK Tg(ACTB-tTA2,-MAPT/lacZ)1Luo/J
006340   STOCK Tg(Gad1-EGFP)98Agmo/J
017000   STOCK Tg(SNCA*E46K)3Elan/J
008474   STOCK Tg(THY1-SNCA*A53T)F53Sud/J
008132   STOCK Tg(THY1-Snca)M1mSud/J
012441   STOCK Tg(tetO-LRRK2*G2019S)E3Cai/J
012442   STOCK Tg(tetO-SNCA*A53T)E2Cai/J
012449   STOCK Tg(teto-LRRK2)C7874Cai/J
View Parkinson's Disease Models     (112 strains)

Strains carrying other alleles of Drd2
020631   B6.129S4(FVB)-Drd2tm1.1Mrub/J
View Strains carrying other alleles of Drd2     (1 strain)

Additional Web Information

Visit the Parkinson's Disease Resource site for helpful information on Parkinson's and research resources.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Myoclonic Dystonia   (DRD2)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Drd2tm1Low/Drd2+

        B6.129S2-Drd2tm1Low
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • mice exhibit a normal saccharin and quinine preference and locomotor depressant response to SCH-23390 treatment   (MGI Ref ID J:50787)
    • abnormal locomotor behavior
      • mice exhibit decreased horizontal distance and rearing compared with C57BL/6 mice   (MGI Ref ID J:47001)
      • ataxia
        • ethanol-treated mice exhibit reduced ataxic response compared with similarly treated wild-type mice   (MGI Ref ID J:50787)
      • decreased vertical activity   (MGI Ref ID J:47001)
      • hypoactivity   (MGI Ref ID J:50787)
    • impaired behavioral response to alcohol
      • ethanol-treated mice exhibit reduced ataxic response compared with similarly treated wild-type mice   (MGI Ref ID J:50787)
  • cardiovascular system phenotype
  • abnormal systemic arterial blood pressure
    • mice exhibit increased blood pressure compared with wild-type mice   (MGI Ref ID J:103181)
    • however, acute adrenalectomy results in normal blood pressure compared with similarly treated wild-type mice   (MGI Ref ID J:103181)
    • increased mean systemic arterial blood pressure   (MGI Ref ID J:103181)
    • increased systemic arterial diastolic blood pressure   (MGI Ref ID J:103181)
    • increased systemic arterial systolic blood pressure   (MGI Ref ID J:103181)
  • growth/size/body phenotype
  • increased body weight
    • compared with wild-type mice or homozygotes   (MGI Ref ID J:103181)

Drd2tm1Low/Drd2tm1Low

        either: B6.129S2-Drd2tm1Low or (involves: 129S2/SvPas * C57BL/6)
  • reproductive system phenotype
  • short uterine horn
    • shorter and thicker than in wild-type mice   (MGI Ref ID J:41858)
  • uterus adenomyosis
    • in 9 of 16 aged female mice   (MGI Ref ID J:41858)
  • uterus cysts
    • in aged female mice   (MGI Ref ID J:41858)
  • uterus hyperplasia
    • in aged female mice   (MGI Ref ID J:41858)
  • nervous system phenotype
  • abnormal pituitary gland morphology
    • pituitary glands exhibit enlarged glandular acini unlike in wild-type mice   (MGI Ref ID J:41858)
    • however, pituitary intermediate lobe size is normal   (MGI Ref ID J:41858)
    • abnormal adenohypophysis morphology
      • older female mice exhibit diffusely enlarged, hyperemic anterior pituitary lobes without focal nodules   (MGI Ref ID J:41858)
      • adenohypophysis peliosis
        • mice exhibit peliosis unlike wild-type mice   (MGI Ref ID J:41858)
      • decreased gonadotroph cell number
        • fewer gonadotrophs stain positive for beta-follicle stimulating hormone and beta-luteinizing hormone compared to in wild-type mice   (MGI Ref ID J:41858)
      • enlarged adenohypophysis
        • in the anterior lobe due to hyperplasia and hypertrophy with prominent vascular spaces   (MGI Ref ID J:41858)
      • increased lactotroph cell number   (MGI Ref ID J:41858)
    • increased pituitary gland weight
      • 4- to 10-fold   (MGI Ref ID J:41858)
  • homeostasis/metabolism phenotype
  • decreased physiological sensitivity to xenobiotic
    • mice exhibit a 3-fold increase in circulating prolactin levels compared with wild-type mice that is insensitive to treatment with the dopamine receptor 2 antagonist haloperidol   (MGI Ref ID J:41858)
  • increased circulating prolactin level
    • mice exhibit a 3-fold increase in circulating prolactin levels compared with wild-type mice that is insensitive to treatment with the dopamine receptor 2 antagonist haloperidol   (MGI Ref ID J:41858)
    • ages female mice exhibit an age-dependent increase in circulating prolactin levels unlike male mice   (MGI Ref ID J:41858)
  • endocrine/exocrine gland phenotype
  • abnormal pituitary gland morphology
    • pituitary glands exhibit enlarged glandular acini unlike in wild-type mice   (MGI Ref ID J:41858)
    • however, pituitary intermediate lobe size is normal   (MGI Ref ID J:41858)
    • abnormal adenohypophysis morphology
      • older female mice exhibit diffusely enlarged, hyperemic anterior pituitary lobes without focal nodules   (MGI Ref ID J:41858)
      • adenohypophysis peliosis
        • mice exhibit peliosis unlike wild-type mice   (MGI Ref ID J:41858)
      • decreased gonadotroph cell number
        • fewer gonadotrophs stain positive for beta-follicle stimulating hormone and beta-luteinizing hormone compared to in wild-type mice   (MGI Ref ID J:41858)
      • enlarged adenohypophysis
        • in the anterior lobe due to hyperplasia and hypertrophy with prominent vascular spaces   (MGI Ref ID J:41858)
      • increased lactotroph cell number   (MGI Ref ID J:41858)
    • increased pituitary gland weight
      • 4- to 10-fold   (MGI Ref ID J:41858)
  • cardiovascular system phenotype
  • adenohypophysis peliosis
    • mice exhibit peliosis unlike wild-type mice   (MGI Ref ID J:41858)

Drd2tm1Low/Drd2tm1Low

        B6.129S2-Drd2tm1Low
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • mice exhibit a normal saccharin and quinine preference and locomotor depressant response to SCH-23390 treatment   (MGI Ref ID J:50787)
    • mice exhibit normal basic motor skills without tremor, ataxia, or abnormal stance or posture   (MGI Ref ID J:103181)
    • mice exhibit normal novel odor habituation and odor sensitivity   (MGI Ref ID J:110704)
    • mice exhibit normal tactile responsivity, trigeminal nerve response, or aversive taste reactivity   (MGI Ref ID J:110704)
    • abnormal latent inhibition of conditioning behavior
      • during reversal learning trials, mice preserve unreinforced behavior and commit more reversal errors across reversal sessions compared with wild-type mice   (MGI Ref ID J:90593)
    • abnormal locomotor behavior
      • mice exhibit decreased horizontal distance, initiation of movement, rearing, and duration of horizontal movement compared with C57BL/6 mice   (MGI Ref ID J:47001)
      • mice exhibit reduced mean distance, number of movements, and time in motion compared with wild-type mice   (MGI Ref ID J:50787)
      • however, the movement speed and movement length are normal   (MGI Ref ID J:50787)
      • abnormal locomotor activation
        • mice exhibit reduced initiation of movement compared with C57BL/6 mice   (MGI Ref ID J:47001)
        • mice exhibit decreased initiation of movement compared with wild-type mice   (MGI Ref ID J:103181)
        • decreased vertical activity   (MGI Ref ID J:47001)
        • hypoactivity   (MGI Ref ID J:50787)
      • ataxia
        • ethanol-treated mice exhibit reduced ataxic response compared with similarly treated wild-type mice   (MGI Ref ID J:50787)
    • abnormal operant conditioning behavior
      • mice exhibit reduced performance in an odor-driven stimulus-discrimination, operant task compared with wild-type mice   (MGI Ref ID J:90593)
    • abnormal response to novel odor
      • mice fail to exhibit an increase in investigation of a novel odor unlike wild-type mice   (MGI Ref ID J:110704)
      • mice exhibit an impairment in olfactory discrimination compared with wild-type mice   (MGI Ref ID J:110704)
      • mice fail to exhibit increased investigation of an object with a novel scent versus one with s familiar scent unlike wild-type mice   (MGI Ref ID J:110704)
      • however, mice exhibit normal exploration behavior   (MGI Ref ID J:110704)
    • alcohol aversion
      • preference ratio is less than 0.4   (MGI Ref ID J:50787)
    • decreased alcohol consumption
      • mice consume less 6% and 10% ethanol solution compared with wild-type mice   (MGI Ref ID J:50787)
    • decreased startle reflex
      • mice exhibit reduced acoustic startle response amplitude compared with wild-type mice   (MGI Ref ID J:154428)
    • impaired behavioral response to addictive substance
      • amphetamine-treated mice fail to exhibit a reduction in prepulse inhibition unlike similarly treated wild-type mice   (MGI Ref ID J:55027)
      • however, amphetamine-treated mice exhibit normal reduction in startle reactivity   (MGI Ref ID J:55027)
      • impaired behavioral response to alcohol
        • ethanol-treated mice fail to exhibit a locomotor depressant responses unlike similarly treated wild-type mice   (MGI Ref ID J:50787)
        • ethanol-treated mice exhibit reduced ataxic response compared with similarly treated wild-type mice   (MGI Ref ID J:50787)
    • impaired coordination
      • on days 2 and 3, but not 4, of a rotarod test   (MGI Ref ID J:47001)
  • nervous system phenotype
  • abnormal CNS synaptic transmission
    • mice fail to exhibit an increase in paired pulse ratio during development unlike wild-type mice   (MGI Ref ID J:127071)
    • mice subjected to high-frequency stimulation fail to exhibit a change in paired pulse ratio unlike similarly treated wild-type mice   (MGI Ref ID J:127071)
    • abnormal excitatory postsynaptic currents
      • mice fail to exhibit a decrease in the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) during development unlike wild-type mice   (MGI Ref ID J:127071)
      • at P21 to 27, mice exhibit increased spontaneous postsynaptic current compared with wild-type mice   (MGI Ref ID J:127071)
    • abnormal prepulse inhibition
      • amphetamine-treated mice fail to exhibit a reduction in prepulse inhibition unlike similarly treated wild-type mice   (MGI Ref ID J:55027)
    • absent long term depression
      • at P22 to 27, striatal long term depression cannot be induced by high-frequency stimulation unlike in wild-type mice   (MGI Ref ID J:127071)
  • abnormal brain development
    • mice fail to exhibit an increase in paired pulse ratio during development unlike wild-type mice   (MGI Ref ID J:127071)
  • respiratory system phenotype
  • decreased pulmonary ventilation
    • in male mice at day 2 and 8 of exposure to poikilocapnic hypoxia   (MGI Ref ID J:130701)
  • increased pulmonary respiratory rate
    • under hypoxic hypercapnic conditions in female, but not male mice   (MGI Ref ID J:130701)
  • increased pulmonary ventilation
    • under hypoxic conditions in female, but not male mice   (MGI Ref ID J:130701)
    • under hypercapnic conditions in male, but not female, mice   (MGI Ref ID J:130701)
    • under hypoxic hypercapnic conditions in female, but not male mice   (MGI Ref ID J:130701)
    • at low levels of hypoxia in male mice   (MGI Ref ID J:130701)
  • increased tidal volume
    • under hypercapnic conditions in male, but not female, mice   (MGI Ref ID J:130701)
    • under hypoxic hypercapnic conditions in female, but not male mice   (MGI Ref ID J:130701)
  • cardiovascular system phenotype
  • abnormal systemic arterial blood pressure
    • mice exhibit increased blood pressure compared with wild-type mice   (MGI Ref ID J:103181)
    • during the first 5 minutes after AT1 antagonist treatment, mice exhibit a greater decrease in blood pressure than similarly treated wild-type mice   (MGI Ref ID J:103181)
    • phentolamine-treated mice exhibit a greater decrease in blood pressure than similarly treated wild-type mice   (MGI Ref ID J:103181)
    • BQ-788-treated mice exhibit a decrease in blood pressure unlike in similarly treated wild-type mice   (MGI Ref ID J:103181)
    • RES-701-1-treated mice exhibit a greater increase in blood pressure than similarly treated wild-type mice   (MGI Ref ID J:103181)
    • sarafotoxin S6c-treated mice exhibit a greater increase in blood pressure than similarly treated wild-type mice   (MGI Ref ID J:103181)
    • however, acute adrenalectomy results in normal blood pressure compared with similarly treated wild-type mice   (MGI Ref ID J:103181)
    • increased mean systemic arterial blood pressure   (MGI Ref ID J:103181)
    • increased systemic arterial diastolic blood pressure   (MGI Ref ID J:103181)
    • increased systemic arterial systolic blood pressure   (MGI Ref ID J:103181)
  • increased heart rate   (MGI Ref ID J:103181)
  • homeostasis/metabolism phenotype
  • increased physiological sensitivity to xenobiotic
    • during the first 5 minutes after AT1 antagonist treatment, mice exhibit a greater decrease in blood pressure than similarly treated wild-type mice   (MGI Ref ID J:103181)
    • phentolamine-treated mice exhibit a greater decrease in blood pressure than similarly treated wild-type mice   (MGI Ref ID J:103181)
    • BQ-788-treated mice exhibit a decrease in blood pressure unlike in similarly treated wild-type mice   (MGI Ref ID J:103181)
    • RES-701-1-treated mice exhibit a greater increase in blood pressure than similarly treated wild-type mice   (MGI Ref ID J:103181)
    • sarafotoxin S6c-treated mice exhibit a greater increase in blood pressure than similarly treated wild-type mice   (MGI Ref ID J:103181)
    • however, mice respond normally to treatment with an ET(A) or V1 vasopressin receptor antagonist   (MGI Ref ID J:103181)
  • increased urine sodium level
    • before and after saline loading   (MGI Ref ID J:103181)
  • renal/urinary system phenotype
  • increased urine sodium level
    • before and after saline loading   (MGI Ref ID J:103181)
  • polyuria
    • before and after saline loading   (MGI Ref ID J:103181)
  • growth/size/body phenotype
  • decreased body weight
    • in male, but not female, mice   (MGI Ref ID J:130701)
  • taste/olfaction phenotype
  • *normal* taste/olfaction phenotype
    • mice exhibit normal novel odor habituation and odor sensitivity   (MGI Ref ID J:110704)

Drd2tm1Low/Drd2tm1Low

        B6.129S2-Drd2tm1Low/J
  • mortality/aging
  • decreased sensitivity to xenobiotic induced morbidity/mortality
    • 4% of methamphetamine-treated mice die compared with 27% of similarly treated wild-type mice   (MGI Ref ID J:137069)
  • homeostasis/metabolism phenotype
  • decreased circulating growth hormone level   (MGI Ref ID J:106832)
  • decreased circulating insulin-like growth factor I level   (MGI Ref ID J:106832)
  • decreased physiological sensitivity to xenobiotic
    • methamphetamine-treated mice fail to exhibit an increase in body temperature unlike similarly treated wild-type mice   (MGI Ref ID J:137069)
  • decreased response to stress-induced hyperthermia
    • methamphetamine-treated mice fail to exhibit an increase in body temperature unlike similarly treated wild-type mice   (MGI Ref ID J:137069)
  • decreased sensitivity to xenobiotic induced morbidity/mortality
    • 4% of methamphetamine-treated mice die compared with 27% of similarly treated wild-type mice   (MGI Ref ID J:137069)
  • increased circulating prolactin level
    • after 3 months in female mice and after 2 months in male mice   (MGI Ref ID J:106832)
  • increased growth hormone level
    • cultured pituitary cells from 4 month old male and female mice release less growth hormone than similarly treated wild-type cells   (MGI Ref ID J:106832)
    • growth hormone releasing hormone (GHRH)-treated pituitary cells from 8 month old mice release less growth hormone than similarly treated wild-type cells   (MGI Ref ID J:106832)
    • however, circulating levels of growth hormone are normal   (MGI Ref ID J:106832)
  • increased susceptibility to dopaminergic neuron neurotoxicity
    • in mice treated with MPTP   (MGI Ref ID J:194407)
  • growth/size/body phenotype
  • decreased body length
    • in male, but not female, mice   (MGI Ref ID J:106832)
  • decreased body weight   (MGI Ref ID J:106832)
  • postnatal growth retardation
    • maximal growth retardation occurs during the first half of the second month of life   (MGI Ref ID J:106832)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • microglia exhibit normal response to LPS   (MGI Ref ID J:194407)
    • abnormal GABAergic neuron morphology
      • at E15, the number of GABA+ cells is increased 44% in the presumptive medial prefrontal cortex compared to in wild-type mice   (MGI Ref ID J:121219)
      • at E15, GABA+ cell density is increased in the intermediate zone 96% compared to in wild-type mice   (MGI Ref ID J:121219)
      • at E15, GABA+ cell density in the ventral zone/subventricular zone is increased 143% compared to in wild-type mice   (MGI Ref ID J:121219)
      • however, the numbers of GABA+ cells in the marginal zone and subplate/cortical plate are normal   (MGI Ref ID J:121219)
    • abnormal astrocyte physiology
      • hyper-responsive to LPS treatment with increased production of pro-inflammatory mediators (as measured by RNA levels)   (MGI Ref ID J:194407)
      • in cultures of astrocytes and mesencephalic dopaminergic neurons, neurons exhibit reduced survival compared to in cultures with wild-type astrocytes   (MGI Ref ID J:194407)
    • abnormal neuronal migration
      • at E15, more neurons enter the cerebral wall compared to in wild-type mice   (MGI Ref ID J:121219)
    • astrocytosis
      • at 2 months in the substantia nigra   (MGI Ref ID J:194407)
      • more severe at 16 months in the substantia nigra and striatum   (MGI Ref ID J:194407)
      • not suppressed by quinpirole in MPTP-treated mice   (MGI Ref ID J:194407)
    • increased susceptibility to dopaminergic neuron neurotoxicity
      • in mice treated with MPTP   (MGI Ref ID J:194407)
    • microgliosis   (MGI Ref ID J:194407)
  • behavior/neurological phenotype
  • abnormal vocalization
    • mice exhibit a longer duration of ultrasonic vocalization compared with wild-type mice   (MGI Ref ID J:134260)
    • however, mice exhibit normal numbers, duration, and bandwidths of ultrasonic vocalizations   (MGI Ref ID J:134260)
  • decreased response to stress-induced hyperthermia
    • methamphetamine-treated mice fail to exhibit an increase in body temperature unlike similarly treated wild-type mice   (MGI Ref ID J:137069)
  • increased food intake
    • relative to body weight, male mice consume more food than wild-type mice   (MGI Ref ID J:106832)
    • however, overall consumption of food is normal   (MGI Ref ID J:106832)
  • adipose tissue phenotype
  • decreased inguinal fat pad weight   (MGI Ref ID J:106832)
  • skeleton phenotype
  • short femur
    • at 15 weeks in male, but not female, mice   (MGI Ref ID J:106832)
  • immune system phenotype
  • decreased spleen weight
    • in male and female mice   (MGI Ref ID J:106832)
  • increased interleukin-1 beta secretion
    • from cultured astrocytes stimulated with conditioned medium of microglia treated with LPS   (MGI Ref ID J:194407)
  • microgliosis   (MGI Ref ID J:194407)
  • limbs/digits/tail phenotype
  • short femur
    • at 15 weeks in male, but not female, mice   (MGI Ref ID J:106832)
  • liver/biliary system phenotype
  • decreased liver weight
    • in male, but not female, mice   (MGI Ref ID J:106832)
  • hematopoietic system phenotype
  • decreased spleen weight
    • in male and female mice   (MGI Ref ID J:106832)
  • microgliosis   (MGI Ref ID J:194407)
  • cellular phenotype
  • abnormal neuronal migration
    • at E15, more neurons enter the cerebral wall compared to in wild-type mice   (MGI Ref ID J:121219)
  • increased susceptibility to dopaminergic neuron neurotoxicity
    • in mice treated with MPTP   (MGI Ref ID J:194407)

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Drd2tm1Low/Drd2+

        involves: 129S2/SvPas * C57BL/6J
  • behavior/neurological phenotype
  • abnormal locomotor behavior
    • mice exhibit abnormal motor function with reduced horizontal distance, initiation of movement, time in motion, and number of rearing events compared with C57BL/6 mice   (MGI Ref ID J:47001)
    • mice treated with SKF38393 and quinpirole exhibit increased horizontal distance compared with similarly treated wild-type mice   (MGI Ref ID J:47001)
  • homeostasis/metabolism phenotype
  • increased physiological sensitivity to xenobiotic
    • mice treated with SKF38393 and quinpirole exhibit increased horizontal distance compared with similarly treated wild-type mice   (MGI Ref ID J:47001)

Drd2tm1Low/Drd2+

        129S/Sv-Drd2tm1Low
  • behavior/neurological phenotype
  • abnormal locomotor behavior
    • mice exhibit decreased horizontal distance compared with 129S/SvEv mice   (MGI Ref ID J:47001)

Drd2tm1Low/Drd2tm1Low

        involves: 129 * C57BL/6
  • behavior/neurological phenotype
  • abnormal locomotor activation
    • mutants do not show lower levels of locomotor stimulation in response to a Grm5 antagonist, MPEP, whereas compared to wild-type controls   (MGI Ref ID J:102700)

Drd2tm1Low/Drd2tm1Low

        129S/Sv-Drd2tm1Low
  • behavior/neurological phenotype
  • abnormal locomotor behavior
    • mice exhibit decreased horizontal distance and initiation of movement compared with 129S/SvEv mice   (MGI Ref ID J:47001)
    • abnormal locomotor activation
      • mice exhibit reduced initiation of movement compared with 129S/SvEv mice   (MGI Ref ID J:47001)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Neurobiology Research
Parkinson's Disease
Receptor Defects
      dopamine receptor

Drd2tm1Low related

Neurobiology Research
Receptor Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Drd2tm1Low
Allele Name targeted mutation 1, Malcolm J Low
Allele Type Targeted (Null/Knockout)
Common Name(s) D2 KO; D2-; D2KO; D2R-; Drd2-;
Mutation Made ByDr. Malcolm Low,   University of Michigan Medical School
Strain of Origin129S2/SvPas
ES Cell Line NameD3
ES Cell Line Strain129S2/SvPas
Gene Symbol and Name Drd2, dopamine receptor D2
Chromosome 9
Gene Common Name(s) D2 receptor; D2DR; D2R; Drd-2;
General Note Unlike mice homozygous for Drd2tm1Ebo mice do not display Phenotypic Similarity to Human Syndrome: Parkinson Disease (J:47001)
Molecular Note A genomic fragment containing exon 7 and part of exon 8 was replaced by a neomycin resistance cassette. [MGI Ref ID J:41858]

Genotyping

Genotyping Information

Genotyping Protocols

Drd2tm1Low STD PCR, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Kelly MA; Rubinstein M; Asa SL; Zhang G; Saez C; Bunzow JR; Allen RG ; Hnasko R ; Ben-Jonathan N ; Grandy DK ; Low MJ. 1997. Pituitary lactotroph hyperplasia and chronic hyperprolactinemia in dopamine D2 receptor-deficient mice. Neuron 19(1):103-13. [PubMed: 9247267]  [MGI Ref ID J:41858]

Additional References

Drd2tm1Low related

Asa SL; Kelly MA; Grandy DK; Low MJ. 1999. Pituitary lactotroph adenomas develop after prolonged lactotroph hyperplasia in dopamine D2 receptor-deficient mice. Endocrinology 140(11):5348-55. [PubMed: 10537166]  [MGI Ref ID J:58342]

Cepeda C; Hurst RS; Altemus KL; Flores-Hernandez J; Calvert CR; Jokel ES; Grandy DK; Low MJ; Rubinstein M; Ariano MA; Levine MS. 2001. Facilitated glutamatergic transmission in the striatum of D2 dopamine receptor-deficient mice. J Neurophysiol 85(2):659-70. [PubMed: 11160501]  [MGI Ref ID J:103965]

Chakroborty D; Chowdhury UR; Sarkar C; Baral R; Dasgupta PS; Basu S. 2008. Dopamine regulates endothelial progenitor cell mobilization from mouse bone marrow in tumor vascularization. J Clin Invest 118(4):1380-9. [PubMed: 18340382]  [MGI Ref ID J:135975]

Chausmer AL; Elmer GI; Rubinstein M; Low MJ; Grandy DK; Katz JL. 2002. Cocaine-induced locomotor activity and cocaine discrimination in dopamine D2 receptor mutant mice. Psychopharmacology (Berl) 163(1):54-61. [PubMed: 12185400]  [MGI Ref ID J:103795]

Chen JF; Moratalla R; Impagnatiello F; Grandy DK; Cuellar B; Rubinstein M; Beilstein MA; Hackett E; Fink JS; Low MJ; Ongini E; Schwarzschild MA. 2001. The role of the D(2) dopamine receptor (D(2)R) in A(2A) adenosine receptor (A(2A)R)-mediated behavioral and cellular responses as revealed by A(2A) and D(2) receptor knockout mice. Proc Natl Acad Sci U S A 98(4):1970-5. [PubMed: 11172060]  [MGI Ref ID J:67550]

Clifford JJ; Kinsella A; Tighe O; Rubinstein M; Grandy DK; Low MJ; Croke DT; Waddington JL. 2001. Comparative, topographically-based evaluation of behavioural phenotype and specification of D(1)-like:D(2) interactions in a line of incipient congenic mice with D(2) dopamine receptor 'knockout'. Neuropsychopharmacology 25(4):527-36. [PubMed: 11557166]  [MGI Ref ID J:106290]

Crandall JE; McCarthy DM; Araki KY; Sims JR; Ren JQ; Bhide PG. 2007. Dopamine receptor activation modulates GABA neuron migration from the basal forebrain to the cerebral cortex. J Neurosci 27(14):3813-22. [PubMed: 17409246]  [MGI Ref ID J:121219]

Cristina C; Diaz-Torga G; Baldi A; Gongora A; Rubinstein M; Low MJ; Becu-Villalobos D. 2005. Increased pituitary vascular endothelial growth factor-a in dopaminergic D2 receptor knockout female mice. Endocrinology 146(7):2952-62. [PubMed: 15817666]  [MGI Ref ID J:129824]

Cristina C; Diaz-Torga G; Gongora A; Guida MC; Perez-Millan MI; Baldi A; Becu-Villalobos D. 2007. Fibroblast growth factor-2 in hyperplastic pituitaries of D2R knockout female mice. Am J Physiol Endocrinol Metab 293(5):E1341-51. [PubMed: 17848635]  [MGI Ref ID J:129379]

Cristina C; Diaz-Torga GS; Goya RG; Kakar SS; Perez-Millan MI; Passos VQ; Giannella-Neto D; Bronstein MD; Becu-Villalobos D. 2007. PTTG expression in different experimental and human prolactinomas in relation to dopaminergic control of lactotropes. Mol Cancer 6:4. [PubMed: 17222350]  [MGI Ref ID J:121484]

Cunningham CL; Howard MA; Gill SJ; Rubinstein M; Low MJ; Grandy DK. 2000. Ethanol-conditioned place preference is reduced in dopamine D2 receptor-deficient mice. Pharmacol Biochem Behav 67(4):693-9. [PubMed: 11166059]  [MGI Ref ID J:102654]

Curry T; Egeto P; Wang H; Podnos A; Wasserman D; Yeomans J. 2013. Dopamine receptor D2 deficiency reduces mouse pup ultrasonic vocalizations and maternal responsiveness. Genes Brain Behav 12(4):397-404. [PubMed: 23521753]  [MGI Ref ID J:213310]

Daigle TL; Wetsel WC; Caron MG. 2011. Opposite function of dopamine D1 and N-methyl-D-aspartate receptors in striatal cannabinoid-mediated signaling. Eur J Neurosci 34(9):1378-89. [PubMed: 22034973]  [MGI Ref ID J:183176]

Darmopil S; Martin AB; De Diego IR; Ares S; Moratalla R. 2009. Genetic inactivation of dopamine D1 but not D2 receptors inhibits L-DOPA-induced dyskinesia and histone activation. Biol Psychiatry 66(6):603-13. [PubMed: 19520364]  [MGI Ref ID J:157276]

Diaz-Torga G; Feierstein C; Libertun C; Gelman D; Kelly MA; Low MJ; Rubinstein M; Becu-Villalobos D. 2002. Disruption of the D2 dopamine receptor alters GH and IGF-I secretion and causes dwarfism in male mice. Endocrinology 143(4):1270-9. [PubMed: 11897683]  [MGI Ref ID J:106832]

Dockstader CL; Rubinstein M; Grandy DK; Low MJ; van der Kooy D. 2001. The D2 receptor is critical in mediating opiate motivation only in opiate-dependent and withdrawn mice. Eur J Neurosci 13(5):995-1001. [PubMed: 11264672]  [MGI Ref ID J:75904]

Dracheva S; Haroutunian V. 2001. Locomotor behavior of dopamine D1 receptor transgenic/D2 receptor deficient hybrid mice. Brain Res 905(1-2):142-51. [PubMed: 11423089]  [MGI Ref ID J:70357]

Elmer GI; Pieper JO; Levy J; Rubinstein M; Low MJ; Grandy DK; Wise RA. 2005. Brain stimulation and morphine reward deficits in dopamine D2 receptor-deficient mice. Psychopharmacology (Berl) 182(1):33-44. [PubMed: 16136297]  [MGI Ref ID J:114311]

Espadas I; Darmopil S; Vergano-Vera E; Ortiz O; Oliva I; Vicario-Abejon C; Martin ED; Moratalla R. 2012. L-DOPA-induced increase in TH-immunoreactive striatal neurons in parkinsonian mice: insights into regulation and function. Neurobiol Dis 48(3):271-81. [PubMed: 22820144]  [MGI Ref ID J:197507]

Fadok JP; Dickerson TM; Palmiter RD. 2009. Dopamine is necessary for cue-dependent fear conditioning. J Neurosci 29(36):11089-97. [PubMed: 19741115]  [MGI Ref ID J:152679]

Fan X; Xu M; Hess EJ. 2010. D2 dopamine receptor subtype-mediated hyperactivity and amphetamine responses in a model of ADHD. Neurobiol Dis 37(1):228-36. [PubMed: 19840852]  [MGI Ref ID J:156905]

Fowler SC; Zarcone TJ; Vorontsova E; Chen R. 2002. Motor and associative deficits in D2 dopamine receptor knockout mice. Int J Dev Neurosci 20(3-5):309-21. [PubMed: 12175868]  [MGI Ref ID J:100036]

Garcia-Tornadu I; Diaz-Torga G; Risso GS; Silveyra P; Cataldi N; Ramirez MC; Low MJ; Libertun C; Becu-Villalobos D. 2009. Hypothalamic orexin, OX1, alphaMSH, NPY and MCRs expression in dopaminergic D2R knockout mice. Neuropeptides 43(4):267-74. [PubMed: 19570576]  [MGI Ref ID J:156563]

Garcia-Tornadu I; Ornstein AM; Chamson-Reig A; Wheeler MB; Hill DJ; Arany E; Rubinstein M; Becu-Villalobos D. 2010. Disruption of the dopamine d2 receptor impairs insulin secretion and causes glucose intolerance. Endocrinology 151(4):1441-50. [PubMed: 20147524]  [MGI Ref ID J:160021]

Granado N; Ares-Santos S; Oliva I; O'Shea E; Martin ED; Colado MI; Moratalla R. 2011. Dopamine D2-receptor knockout mice are protected against dopaminergic neurotoxicity induced by methamphetamine or MDMA. Neurobiol Dis 42(3):391-403. [PubMed: 21303698]  [MGI Ref ID J:172768]

Grieder TE; George O; Tan H; George SR; Le Foll B; Laviolette SR; van der Kooy D. 2012. Phasic D1 and tonic D2 dopamine receptor signaling double dissociate the motivational effects of acute nicotine and chronic nicotine withdrawal. Proc Natl Acad Sci U S A 109(8):3101-6. [PubMed: 22308372]  [MGI Ref ID J:182622]

Halberstadt AL; Geyer MA. 2009. Habituation and sensitization of acoustic startle: opposite influences of dopamine D1 and D2-family receptors. Neurobiol Learn Mem 92(2):243-8. [PubMed: 18644244]  [MGI Ref ID J:154428]

Hayward MD; Low MJ. 2005. Naloxone's suppression of spontaneous and food-conditioned locomotor activity is diminished in mice lacking either the dopamine D(2) receptor or enkephalin. Brain Res Mol Brain Res 140(1-2):91-8. [PubMed: 16125819]  [MGI Ref ID J:124309]

Hentges ST; Low MJ. 2002. Ovarian dependence for pituitary tumorigenesis in d2 dopamine receptor-deficient mice. Endocrinology 143(12):4536-43. [PubMed: 12446580]  [MGI Ref ID J:80287]

Herrmann R; Heflin SJ; Hammond T; Lee B; Wang J; Gainetdinov RR; Caron MG; Eggers ED; Frishman LJ; McCall MA; Arshavsky VY. 2011. Rod vision is controlled by dopamine-dependent sensitization of rod bipolar cells by GABA. Neuron 72(1):101-10. [PubMed: 21982372]  [MGI Ref ID J:178532]

Huey KA; Low MJ; Kelly MA; Juarez R; Szewczak JM; Powell FL. 2000. Ventilatory responses to acute and chronic hypoxia in mice: effects of dopamine D(2) receptors. J Appl Physiol 89(3):1142-50. [PubMed: 10956362]  [MGI Ref ID J:130701]

Ito M; Numachi Y; Ohara A; Sora I. 2008. Hyperthermic and lethal effects of methamphetamine: Roles of dopamine D1 and D2 receptors. Neurosci Lett 438(3):327-9. [PubMed: 18486343]  [MGI Ref ID J:137069]

Kachroo A; Orlando LR; Grandy DK; Chen JF; Young AB; Schwarzschild MA. 2005. Interactions between metabotropic glutamate 5 and adenosine A2A receptors in normal and parkinsonian mice. J Neurosci 25(45):10414-9. [PubMed: 16280580]  [MGI Ref ID J:102700]

Kelly MA; Low MJ; Rubinstein M; Phillips TJ. 2008. Role of dopamine D1-like receptors in methamphetamine locomotor responses of D2 receptor knockout mice. Genes Brain Behav 7(5):568-77. [PubMed: 18363855]  [MGI Ref ID J:150099]

Kelly MA; Rubinstein M; Phillips TJ; Lessov CN; Burkhart-Kasch S; Zhang G; Bunzow JR; Fang Y; Gerhardt GA; Grandy DK; Low MJ. 1998. Locomotor activity in D2 dopamine receptor-deficient mice is determined by gene dosage, genetic background, and developmental adaptations. J Neurosci 18(9):3470-9. [PubMed: 9547254]  [MGI Ref ID J:47001]

Kim KS; Yoon YR; Lee HJ; Yoon S; Kim SY; Shin SW; An JJ; Kim MS; Choi SY; Sun W; Baik JH. 2010. Enhanced hypothalamic leptin signaling in mice lacking dopamine D2 receptors. J Biol Chem 285(12):8905-17. [PubMed: 20080963]  [MGI Ref ID J:161078]

Klinker F; Hasan K; Paulus W; Nitsche MA; Liebetanz D. 2013. Pharmacological blockade and genetic absence of the dopamine D2 receptor specifically modulate voluntary locomotor activity in mice. Behav Brain Res 242:117-24. [PubMed: 23291158]  [MGI Ref ID J:197062]

Kruzich PJ; Grandy DK. 2004. Dopamine D2 receptors mediate two-odor discrimination and reversal learning in C57BL/6 mice. BMC Neurosci 5(1):12. [PubMed: 15061865]  [MGI Ref ID J:90593]

Kuchenbauer F; Theodoropoulou M; Hopfner U; Stalla J; Renner U; Tonn JC; Low MJ; Arzt E; Stalla GK; Paez-Pereda M. 2003. Laminin inhibits lactotroph proliferation and is reduced in early prolactinoma development. Mol Cell Endocrinol 207(1-2):13-20. [PubMed: 12972179]  [MGI Ref ID J:126844]

Kvajo M; McKellar H; Gogos JA. 2012. Avoiding mouse traps in schizophrenia genetics: lessons and promises from current and emerging mouse models. Neuroscience 211:136-64. [PubMed: 21821099]  [MGI Ref ID J:184660]

Li XX; Bek M; Asico LD; Yang Z; Grandy DK; Goldstein DS; Rubinstein M; Eisner GM; Jose PA. 2001. Adrenergic and endothelin B receptor-dependent hypertension in dopamine receptor type-2 knockout mice. Hypertension 38(3):303-8. [PubMed: 11566895]  [MGI Ref ID J:103181]

Maison SF; Liu XP; Eatock RA; Sibley DR; Grandy DK; Liberman MC. 2012. Dopaminergic Signaling in the Cochlea: Receptor Expression Patterns and Deletion Phenotypes. J Neurosci 32(1):344-355. [PubMed: 22219295]  [MGI Ref ID J:179360]

Murer MG; Dziewczapolski G; Salin P; Vila M; Tseng KY; Ruberg M; Rubinstein M; Kelly MA; Grandy DK; Low MJ; Hirsch E; Raisman-Vozari R; Gershanik O. 2000. The indirect basal ganglia pathway in dopamine D(2) receptor-deficient mice. Neuroscience 99(4):643-50. [PubMed: 10974427]  [MGI Ref ID J:119592]

Narayanan S; Lam H; Christian L; Levine MS; Grandy D; Rubinstein M; Maidment NT. 2004. Endogenous opioids mediate basal hedonic tone independent of dopamine D-1 or D-2 receptor activation. Neuroscience 124(1):241-6. [PubMed: 14960355]  [MGI Ref ID J:90516]

Neve KA; Ford CP; Buck DC; Grandy DK; Neve RL; Phillips TJ. 2013. Normalizing dopamine D2 receptor-mediated responses in D2 null mutant mice by virus-mediated receptor restoration: Comparing D2 and D2 Neuroscience 248C:479-487. [PubMed: 23811070]  [MGI Ref ID J:207056]

Ogilvie JM; Hakenewerth AM; Gardner RR; Martak JG; Maggio VM. 2009. Dopamine receptor loss of function is not protective of rd1 rod photoreceptors in vivo. Mol Vis 15:2868-78. [PubMed: 20038975]  [MGI Ref ID J:157088]

Palmer AA; Low MJ; Grandy DK; Phillips TJ. 2003. Effects of a Drd2 deletion mutation on ethanol-induced locomotor stimulation and sensitization suggest a role for epistasis. Behav Genet 33(3):311-24. [PubMed: 12837020]  [MGI Ref ID J:103087]

Phillips TJ; Brown KJ; Burkhart-Kasch S; Wenger CD; Kelly MA; Rubinstein M; Grandy DK; Low MJ. 1998. Alcohol preference and sensitivity are markedly reduced in mice lacking dopamine D2 receptors. Nat Neurosci 1(7):610-5. [PubMed: 10196569]  [MGI Ref ID J:50787]

Prieto-Lloret J; Donnelly DF; Rico AJ; Moratalla R; Gonzalez C; Rigual RJ. 2007. Hypoxia transduction by carotid body chemoreceptors in mice lacking dopamine D(2) receptors. J Appl Physiol 103(4):1269-75. [PubMed: 17673562]  [MGI Ref ID J:147533]

Ralph RJ; Varty GB; Kelly MA; Wang YM; Caron MG; Rubinstein M ; Grandy DK ; Low MJ ; Geyer MA. 1999. The dopamine D2, but not D3 or D4, receptor subtype is essential for the disruption of prepulse inhibition produced by amphetamine in mice. J Neurosci 19(11):4627-33. [PubMed: 10341260]  [MGI Ref ID J:55027]

Ralph-Williams RJ; Lehmann-Masten V; Otero-Corchon V; Low MJ; Geyer MA. 2002. Differential effects of direct and indirect dopamine agonists on prepulse inhibition: a study in D1 and D2 receptor knock-out mice. J Neurosci 22(21):9604-11. [PubMed: 12417685]  [MGI Ref ID J:111572]

Recouvreux MV; Guida MC; Rifkin DB; Becu-Villalobos D; Diaz-Torga G. 2011. Active and total transforming growth factor-{beta}1 are differentially regulated by dopamine and estradiol in the pituitary. Endocrinology 152(7):2722-30. [PubMed: 21521749]  [MGI Ref ID J:174905]

Recouvreux MV; Lapyckyj L; Camilletti MA; Guida MC; Ornstein A; Rifkin DB; Becu-Villalobos D; Diaz-Torga G. 2013. Sex differences in the pituitary transforming growth factor-beta1 system: studies in a model of resistant prolactinomas. Endocrinology 154(11):4192-205. [PubMed: 24008346]  [MGI Ref ID J:203821]

Risinger FO; Freeman PA; Rubinstein M; Low MJ; Grandy DK. 2000. Lack of operant ethanol self-administration in dopamine D2 receptor knockout mice. Psychopharmacology (Berl) 152(3):343-50. [PubMed: 11105945]  [MGI Ref ID J:103899]

Schuff KG; Hentges ST; Kelly MA; Binart N; Kelly PA; Iuvone PM; Asa SL; Low MJ. 2002. Lack of prolactin receptor signaling in mice results in lactotroph proliferation and prolactinomas by dopamine-dependent and -independent mechanisms. J Clin Invest 110(7):973-81. [PubMed: 12370275]  [MGI Ref ID J:79683]

Shao W; Zhang SZ; Tang M; Zhang XH; Zhou Z; Yin YQ; Zhou QB; Huang YY; Liu YJ; Wawrousek E; Chen T; Li SB; Xu M; Zhou JN; Hu G; Zhou JW. 2013. Suppression of neuroinflammation by astrocytic dopamine D2 receptors via alphaB-crystallin. Nature 494(7435):90-4. [PubMed: 23242137]  [MGI Ref ID J:194407]

Sturgess JE; Ting-A-Kee RA; Podbielski D; Sellings LH; Chen JF; van der Kooy D. 2010. Adenosine A1 and A2A receptors are not upstream of caffeine's dopamine D2 receptor-dependent aversive effects and dopamine-independent rewarding effects. Eur J Neurosci 32(1):143-54. [PubMed: 20576036]  [MGI Ref ID J:171784]

Tang K; Low MJ; Grandy DK; Lovinger DM. 2001. Dopamine-dependent synaptic plasticity in striatum during in vivo development. Proc Natl Acad Sci U S A 98(3):1255-60. [PubMed: 11158626]  [MGI Ref ID J:127071]

Tillerson JL; Caudle WM; Parent JM; Gong C; Schallert T; Miller GW. 2006. Olfactory discrimination deficits in mice lacking the dopamine transporter or the D2 dopamine receptor. Behav Brain Res 172(1):97-105. [PubMed: 16765459]  [MGI Ref ID J:110704]

Ting-A-Kee R; Dockstader C; Heinmiller A; Grieder T; van der Kooy D. 2009. GABA(A) receptors mediate the opposing roles of dopamine and the tegmental pedunculopontine nucleus in the motivational effects of ethanol. Eur J Neurosci 29(6):1235-44. [PubMed: 19302158]  [MGI Ref ID J:147193]

Tseng KY; Roubert C; Do L; Rubinstein M; Kelly MA; Grandy DK; Low MJ; Gershanik OS; Murer MG; Giros B; Raisman-Vozari R. 2000. Selective increase of Nurr1 mRNA expression in mesencephalic dopaminergic neurons of D2 dopamine receptor-deficient mice Brain Res Mol Brain Res 80(1):1-6. [PubMed: 11039723]  [MGI Ref ID J:64369]

Villar-Cheda B; Dominguez-Meijide A; Valenzuela R; Granado N; Moratalla R; Labandeira-Garcia JL. 2014. Aging-related dysregulation of dopamine and angiotensin receptor interaction. Neurobiol Aging 35(7):1726-38. [PubMed: 24529758]  [MGI Ref ID J:213879]

Vinkers CH; Risbrough VB; Geyer MA; Caldwell S; Low MJ; Hauger RL. 2007. Role of dopamine D1 and D2 receptors in CRF-induced disruption of sensorimotor gating. Pharmacol Biochem Behav 86(3):550-8. [PubMed: 17324452]  [MGI Ref ID J:124479]

Vohra PK; Hoeppner LH; Sagar G; Dutta SK; Misra S; Hubmayr RD; Mukhopadhyay D. 2012. Dopamine inhibits pulmonary edema through the VEGF-VEGFR2 axis in a murine model of acute lung injury. Am J Physiol Lung Cell Mol Physiol 302(2):L185-92. [PubMed: 22003095]  [MGI Ref ID J:183327]

Wang H; Liang S; Burgdorf J; Wess J; Yeomans J. 2008. Ultrasonic vocalizations induced by sex and amphetamine in M2, M4, M5 muscarinic and D2 dopamine receptor knockout mice. PLoS ONE 3(4):e1893. [PubMed: 18382674]  [MGI Ref ID J:134260]

Wang HD; Stanwood GD; Grandy DK; Deutch AY. 2009. Dystrophic dendrites in prefrontal cortical pyramidal cells of dopamine D1 and D2 but not D4 receptor knockout mice. Brain Res 1300:58-64. [PubMed: 19747903]  [MGI Ref ID J:157411]

Yoon S; Baik JH. 2013. Dopamine D2 receptor-mediated epidermal growth factor receptor transactivation through a disintegrin and metalloprotease regulates dopaminergic neuron development via extracellular signal-related kinase activation. J Biol Chem 288(40):28435-46. [PubMed: 23955337]  [MGI Ref ID J:203838]

Yoon S; Choi MH; Chang MS; Baik JH. 2011. Wnt5a-Dopamine D2 Receptor Interactions Regulate Dopamine Neuron Development via Extracellular Signal-regulated Kinase (ERK) Activation. J Biol Chem 286(18):15641-51. [PubMed: 21454669]  [MGI Ref ID J:172250]

Zahniser NR; Simosky JK; Mayfield RD; Negri CA; Hanania T; Larson GA; Kelly MA; Grandy DK; Rubinstein M; Low MJ; Fredholm BB. 2000. Functional uncoupling of adenosine A(2A) receptors and reduced responseto caffeine in mice lacking dopamine D2 receptors. J Neurosci 20(16):5949-57. [PubMed: 10934242]  [MGI Ref ID J:112280]

Zhang Y; Cuevas S; Asico LD; Escano C; Yang Y; Pascua AM; Wang X; Jones JE; Grandy D; Eisner G; Jose PA; Armando I. 2012. Deficient dopamine D2 receptor function causes renal inflammation independently of high blood pressure. PLoS One 7(6):e38745. [PubMed: 22719934]  [MGI Ref ID J:187830]

Health & husbandry

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Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

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Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2525.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3283.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

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.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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