Strain Name:

STOCK Drd1atm1Jcd/J

Stock Number:

002322

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Cryopreserved - Ready for recovery

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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 Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
 
Donating InvestigatorDr. Heiner Westphal,   National Institutes of Health

Description
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 Homozygotes do appear thinner than wildtypes and have a very slight halting gait (unpublished observations, The Jackson Laboratory).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.

Development
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. 129-derived J1 ES cells were used.

Control Information

  Control
   None Available
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Drd1atm1Jcd allele
002959   B6.129S4-Drd1atm1Jcd/J
View Strains carrying   Drd1atm1Jcd     (1 strain)

Strains carrying other alleles of Drd1a
016204   B6.Cg-Tg(Drd1a-tdTomato)6Calak/J
007586   B6;129S4-Drd1atm2Rpa/J
018156   STOCK Tg(Drd1a-rtTA)ARgmk/J
View Strains carrying other alleles of Drd1a     (3 strains)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Drd1atm1Jcd/Drd1a+

        involves: 129S4/SvJae
  • behavior/neurological phenotype
  • abnormal contextual conditioning behavior
    • 3-5 month old mice exhibit delayed extinction of conditioned fear responses compared to wild-type; mice display normal acquisition of contextual fear conditioning; null mice do not show a decline in freeaing responses over three days as do the wild-type; a significantly higher her percentage of contextual freezing responses is observed for up to 90 days   (MGI Ref ID J:67395)
  • abnormal passive avoidance behavior
    • after confinement for 1 minute to the shock-paired chamber, 3 to 5 month old heterozygous mice show less of a decline in latency to enter the conditioning chamber compared to wild-type   (MGI Ref ID J:67395)

Drd1atm1Jcd/Drd1atm1Jcd

        involves: 129S4/SvJae * C57BL/6
  • mortality/aging
  • premature death
    • majority of mice die within 1 week after weaning unless given hydrated food   (MGI Ref ID J:22076)
  • behavior/neurological phenotype
  • decreased vertical activity
    • 5-6 week old mutants exhibit significantly fewer rearing events than wild-type   (MGI Ref ID J:22076)
  • hunched posture
    • by weaning, mice have hunched posture   (MGI Ref ID J:22076)
  • growth/size/body phenotype
  • decreased body weight
    • mice that are separated from heterozygous and wild-type littermates fed moistened lab chow appear healthy but only gain 70% of weight that sex-matched littermates reach by 6 weeks of age   (MGI Ref ID J:22076)
  • postnatal growth retardation
    • mice are normal with respect to wild-type up to 2 weeks of age, but are significantly growth retarded by weaning age; mice appear sickly and majority do not gain weight   (MGI Ref ID J:22076)
  • integument phenotype
  • disheveled coat
    • by weaning, mice have poorly groomed coat   (MGI Ref ID J:22076)

Drd1atm1Jcd/Drd1atm1Jcd

        involves: 129S4/SvJae
  • behavior/neurological phenotype
  • abnormal contextual conditioning behavior
    • 3-5 month old mice exhibit delayed extinction of conditioned fear responses compared to wild-type; mice display normal acquisition of contextual fear conditioning; null mice do not show a decline in freeaing responses over three days as do the wild-type; a significantly higher her percentage of contextual freezing responses is observed for up to 90 days   (MGI Ref ID J:67395)
  • abnormal passive avoidance behavior
    • 3-5 month old nulls maintain enhanced step-through latencies for up to 45 days post shock-conditioning   (MGI Ref ID J:67395)
    • after confinement for 1 minute to the shock-paired chamber, null mice show less of a decline in latency to enter the conditioning chamber compared to wild-type   (MGI Ref ID J:67395)
  • abnormal spatial learning
    • 3-5 month old null mice exhibit a spatial learning deficit as shown by longer latencies to locate a hidden platmform in the initial acquisition phase   (MGI Ref ID J:102603)
    • in the first probe trial with an absent platform conducted 24 hours after the acquisiton trials, null mice display less selective searching behavior for an absent platform and less time in the target quadrant (40% for control, 27% for nulls); on reversal trials with the platform in a new location, null animals have longer escape latencies than control over the course of 12 trials   (MGI Ref ID J:102603)
    • in a second probe trial with the platform removed, the time spent in the target quadrant by null mice is 31% compared to 50% by controls and had a reduced number of annulus crossings through the former location of the platform   (MGI Ref ID J:102603)
    • in trials with a visual cue of the platform location, null mice showed longer escape latencies during trials 4-12, then showed similar performance to conrols   (MGI Ref ID J:102603)
    • in a Morris water maze   (MGI Ref ID J:102600)
  • behavioral despair
    • mice tend to float in the water instead of swimming compared with wild-type mice   (MGI Ref ID J:102600)
  • decreased vertical activity   (MGI Ref ID J:102600)
  • hypoactivity
    • in an open field compared with wild-type mice   (MGI Ref ID J:102600)
  • impaired coordination
    • compared with wild-type mice   (MGI Ref ID J:102600)
  • increased thigmotaxis
  • nervous system phenotype
  • abnormal neuronal migration
    • at E15, fewer neurons enter the cerebral wall compared to in wild-type mice   (MGI Ref ID J:121219)
  • loss of GABAergic neurons
    • at E15, the number of GABA+ cells is decreased 25% in the presumptive medial prefrontal cortex compared to in wild-type mice   (MGI Ref ID J:121219)
    • at E15, GABA+ cell density is decreased in the intermediate zone 48% compared to in wild-type mice   (MGI Ref ID J:121219)
    • at E15, GABA+ cell density in the ventral zone/subventricular zone is decreased 53% 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)
  • growth/size/body phenotype
  • decreased body size   (MGI Ref ID J:102603)
    • nulls are 20-30% smaller than heterozygotes or wild-type   (MGI Ref ID J:67395)
  • cellular phenotype
  • abnormal neuronal migration
    • at E15, fewer neurons enter the cerebral wall compared to in wild-type mice   (MGI Ref ID J:121219)

Drd1atm1Jcd/Drd1atm1Jcd

        B6.129S4-Drd1atm1Jcd/J
  • mortality/aging
  • decreased sensitivity to xenobiotic induced morbidity/mortality
    • 7% of methamphetamine-treated mice die compared with 27% of similarly treated wild-type mice   (MGI Ref ID J:137069)
  • homeostasis/metabolism phenotype
  • decreased physiological sensitivity to xenobiotic
    • methamphetamine-treated mice exhibit less of an increase in body temperature compared with similarly treated wild-type mice   (MGI Ref ID J:137069)
  • decreased response to stress-induced hyperthermia
    • methamphetamine-treated mice exhibit less of an increase in body temperature compared with similarly treated wild-type mice   (MGI Ref ID J:137069)
  • decreased sensitivity to xenobiotic induced morbidity/mortality
    • 7% of methamphetamine-treated mice die compared with 27% of similarly treated wild-type mice   (MGI Ref ID J:137069)
  • vision/eye phenotype
  • abnormal eye electrophysiology
    • baseline amplitude of the light-adapted electroretinographic response is reduced   (MGI Ref ID J:185955)
  • abnormal vision
    • visual acuity is reduced   (MGI Ref ID J:185955)
    • small increase in contrast sensitivity at high spatial frequencies   (MGI Ref ID J:185955)
  • behavior/neurological phenotype
  • decreased response to stress-induced hyperthermia
    • methamphetamine-treated mice exhibit less of an increase in body temperature compared with similarly treated wild-type mice   (MGI Ref ID J:137069)

Drd1atm1Jcd/Drd1atm1Jcd

        B6.129S4-Drd1atm1Jcd
  • behavior/neurological phenotype
  • increased startle reflex
    • mice exhibit increased acoustic startle response amplitude compared with wild-type mice   (MGI Ref ID J:154428)
View Research Applications

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

Neurobiology Research
Receptor Defects
      dopamine receptor

Drd1atm1Jcd related

Neurobiology Research
Cortical Defects
Neurotransmitter Receptor and Synaptic Vesicle Defects
Receptor Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Drd1atm1Jcd
Allele Name targeted mutation 1, John Drago
Allele Type Targeted (Null/Knockout)
Common Name(s) D1-; D1A-; D1r-;
Mutation Made ByDr. John Drago,   National Institutes of Health
Strain of Origin129S4/SvJae
ES Cell Line NameJ1
ES Cell Line Strain129S4/SvJae
Gene Symbol and Name Drd1a, dopamine receptor D1A
Chromosome 13
Gene Common Name(s) C030036C15Rik; D1 receptor; D1a; DADR; Drd-1; Drd1; G-protein coupled receptor 15; Gpcr15; RIKEN cDNA C030036C15 gene; dopamine receptor 1;
Molecular Note A neomycin resistance cassette replaced 0.75kb of sequence encoding the fifth transmembrane domain and third intracytoplasmic loop. [MGI Ref ID J:22076]

Genotyping

Genotyping Information

Genotyping Protocols

Drd1atm1Jcd, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Drago J; Gerfen CR; Lachowicz JE; Steiner H; Hollon TR; Love PE; Ooi GT; Grinberg A; Lee EJ; Huang SP; Bartlett PF; Jose PA; Sibley DR; Westphal H. 1994. Altered striatal function in a mutant mouse lacking D1A dopamine receptors. Proc Natl Acad Sci U S A 91(26):12564-8. [PubMed: 7809078]  [MGI Ref ID J:22076]

Additional References

Levine MS; Altemus KL; Cepeda C; Cromwell HC; Crawford C; Ariano MA; Drago J; Sibley DR; Westphal H. 1996. Modulatory actions of dopamine on NMDA receptor-mediated responses are reduced in D1A-deficient mutant mice. J Neurosci 16(18):5870-82. [PubMed: 8795639]  [MGI Ref ID J:35286]

Drd1atm1Jcd related

Beaulieu JM; Tirotta E; Sotnikova TD; Masri B; Salahpour A; Gainetdinov RR; Borrelli E; Caron MG. 2007. Regulation of Akt signaling by D2 and D3 dopamine receptors in vivo. J Neurosci 27(4):881-5. [PubMed: 17251429]  [MGI Ref ID J:117785]

Bender M; Drago J; Rivkees SA. 1997. D1 receptors mediate dopamine action in the fetal suprachiasmatic nuclei: studies of mice with targeted deletion of the D1 dopamine receptor gene. Brain Res Mol Brain Res 49(1-2):271-7. [PubMed: 9387887]  [MGI Ref ID J:43604]

Cannon CM; Scannell CA; Palmiter RD. 2005. Mice lacking dopamine D1 receptors express normal lithium chloride-induced conditioned taste aversion for salt but not sucrose. Eur J Neurosci 21(9):2600-4. [PubMed: 15932618]  [MGI Ref ID J:101069]

Clifford JJ; Tighe O; Croke DT; Kinsella A; Sibley DR; Drago J; Waddington JL. 1999. Conservation of behavioural topography to dopamine D1-like receptor agonists in mutant mice lacking the D1A receptor implicates a D1-like receptor not coupled to adenylyl cyclase. Neuroscience 93(4):1483-9. [PubMed: 10501473]  [MGI Ref ID J:59466]

Clifford JJ; Tighe O; Croke DT; Sibley DR; Drago J; Waddington JL. 1998. Topographical evaluation of the phenotype of spontaneous behaviour in mice with targeted gene deletion of the D1A dopamine receptor: paradoxical elevation of grooming syntax. Neuropharmacology 37(12):1595-602. [PubMed: 9886682]  [MGI Ref ID J:52350]

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]

Crawford CA; Drago J; Watson JB; Levine MS. 1997. Effects of repeated amphetamine treatment on the locomotor activity of the dopamine D1A-deficient mouse. Neuroreport 8(11):2523-7. [PubMed: 9261820]  [MGI Ref ID J:45740]

Cromwell HC; Berridge KC; Drago J; Levine MS. 1998. Action sequencing is impaired in D1A-deficient mutant mice. Eur J Neurosci 10(7):2426-32. [PubMed: 9749770]  [MGI Ref ID J:50990]

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]

Drago F; Contarino A; Busa L. 1999. The expression of neuropeptide-induced excessive grooming behavior in dopamine D1 and D2 receptor-deficient mice. Eur J Pharmacol 365(2-3):125-31. [PubMed: 9988094]  [MGI Ref ID J:56015]

El-Ghundi M; Fletcher PJ; Drago J; Sibley DR; O'Dowd BF; George SR. 1999. Spatial learning deficit in dopamine D(1) receptor knockout mice. Eur J Pharmacol 383(2):95-106. [PubMed: 10585522]  [MGI Ref ID J:102603]

El-Ghundi M; O'Dowd BF; Erclik M; George SR. 2003. Attenuation of sucrose reinforcement in dopamine D1 receptor deficient mice. Eur J Neurosci 17(4):851-62. [PubMed: 12603275]  [MGI Ref ID J:107997]

El-Ghundi M; O'Dowd BF; George SR. 2001. Prolonged fear responses in mice lacking dopamine D(1) receptor. Brain Res 892(1):86-93. [PubMed: 11172752]  [MGI Ref ID J:67395]

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]

Friedman E; Jin LQ; Cai GP; Hollon TR; Drago J; Sibley DR; Wang HY. 1997. D1-like dopaminergic activation of phosphoinositide hydrolysis is independent of D1A dopamine receptors: evidence from D1A knockout mice. Mol Pharmacol 51(1):6-11. [PubMed: 9016340]  [MGI Ref ID J:38464]

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]

He Q; Xu HP; Wang P; Tian N. 2013. Dopamine D1 receptors regulate the light dependent development of retinal synaptic responses. PLoS One 8(11):e79625. [PubMed: 24260267]  [MGI Ref ID J:209679]

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]

Herve D; Le Moine C; Corvol JC; Belluscio L; Ledent C; Fienberg AA; Jaber M; Studler JM; Girault JA. 2001. Galpha(olf) levels are regulated by receptor usage and control dopamine and adenosine action in the striatum. J Neurosci 21(12):4390-9. [PubMed: 11404425]  [MGI Ref ID J:123805]

Huang YY; Simpson E; Kellendonk C; Kandel ER. 2004. Genetic evidence for the bidirectional modulation of synaptic plasticity in the prefrontal cortex by D1 receptors. Proc Natl Acad Sci U S A 101(9):3236-41. [PubMed: 14981263]  [MGI Ref ID J:88654]

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]

Jackson CR; Ruan GX; Aseem F; Abey J; Gamble K; Stanwood G; Palmiter RD; Iuvone PM; McMahon DG. 2012. Retinal Dopamine Mediates Multiple Dimensions of Light-Adapted Vision. J Neurosci 32(27):9359-9368. [PubMed: 22764243]  [MGI Ref ID J:185955]

Karasinska JM; George SR; Cheng R; O'Dowd BF. 2005. Deletion of dopamine D1 and D3 receptors differentially affects spontaneous behaviour and cocaine-induced locomotor activity, reward and CREB phosphorylation. Eur J Neurosci 22(7):1741-50. [PubMed: 16197514]  [MGI Ref ID J:102922]

Karasinska JM; George SR; El-Ghundi M; Fletcher PJ; O'Dowd BF. 2000. Modification of dopamine D(1) receptor knockout phenotype in mice lacking both dopamine D(1) and D(3) receptors. Eur J Pharmacol 399(2-3):171-81. [PubMed: 10884517]  [MGI Ref ID J:102600]

Karper PE; De la Rosa H; Newman ER; Krall CM; Nazarian A; McDougall SA; Crawford CA. 2002. Role of D1-like receptors in amphetamine-induced behavioral sensitization: a study using D1A receptor knockout mice. Psychopharmacology (Berl) 159(4):407-14. [PubMed: 11823893]  [MGI Ref ID J:103950]

Karper PE; Nazarian A; Crawford CA; Drago J; McDougall SA. 2000. Role of dopamine D(1) receptors for kappa-opioid-mediated locomotor activity and antinociception during the preweanling period: a study using D(1) receptor knockout mice. Physiol Behav 68(4):585-90. [PubMed: 10713301]  [MGI Ref ID J:96590]

Kobayashi M; Iaccarino C; Saiardi A; Heidt V; Bozzi Y; Picetti R; Vitale C; Westphal H; Drago J; Borrelli E. 2004. Simultaneous absence of dopamine D1 and D2 receptor-mediated signaling is lethal in mice. Proc Natl Acad Sci U S A 101(31):11465-70. [PubMed: 15272078]  [MGI Ref ID J:91781]

Leonard SK; Ferry-Leeper P; Mailman RB. 2006. Low affinity binding of the classical D(1) antagonist SCH23390 in rodent brain: Potential interaction with A(2A) and D(2)-like receptors. Brain Res 1117(1):25-37. [PubMed: 16962565]  [MGI Ref ID J:114543]

Levine MS; Altemus KL; Cepeda C; Cromwell HC; Crawford C; Ariano MA; Drago J; Sibley DR; Westphal H. 1996. Modulatory actions of dopamine on NMDA receptor-mediated responses are reduced in D1A-deficient mutant mice. J Neurosci 16(18):5870-82. [PubMed: 8795639]  [MGI Ref ID J:35286]

Liedtke WB; McKinley MJ; Walker LL; Zhang H; Pfenning AR; Drago J; Hochendoner SJ; Hilton DL; Lawrence AJ; Denton DA. 2011. Relation of addiction genes to hypothalamic gene changes subserving genesis and gratification of a classic instinct, sodium appetite. Proc Natl Acad Sci U S A 108(30):12509-14. [PubMed: 21746918]  [MGI Ref ID J:174535]

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]

Matthies H; Becker A; Schroeder H; Kraus J; Hollt V; Krug M. 1997. Dopamine D1-deficient mutant mice do not express the late phase of hippocampal long-term potentiation. Neuroreport 8(16):3533-5. [PubMed: 9427321]  [MGI Ref ID J:103731]

McNamara FN; Clifford JJ; Tighe O; Kinsella A; Drago J; Croke DT; Waddington JL. 2003. Congenic D1A dopamine receptor mutants: ethologically based resolution of behavioural topography indicates genetic background as a determinant of knockout phenotype. Neuropsychopharmacology 28(1):86-99. [PubMed: 12496944]  [MGI Ref ID J:106126]

Miner LL; Drago J; Chamberlain PM; Donovan D; Uhl GR. 1995. Retained cocaine conditioned place preference in D1 receptor deficient mice. Neuroreport 6(17):2314-6. [PubMed: 8747144]  [MGI Ref ID J:117915]

Miyamoto S; Mailman RB; Lieberman JA; Duncan GE. 2001. Blunted brain metabolic response to ketamine in mice lacking D(1A) dopamine receptors. Brain Res 894(2):167-80. [PubMed: 11251190]  [MGI Ref ID J:68124]

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]

Ng J; Rashid AJ; So CH; O'Dowd BF; George SR. 2010. Activation of calcium/calmodulin-dependent protein kinase IIalpha in the striatum by the heteromeric D1-D2 dopamine receptor complex. Neuroscience 165(2):535-41. [PubMed: 19837142]  [MGI Ref ID J:158207]

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]

Parish CL; Finkelstein DI; Drago J; Borrelli E; Horne MK. 2001. The role of dopamine receptors in regulating the size of axonal arbors. J Neurosci 21(14):5147-57. [PubMed: 11438590]  [MGI Ref ID J:70177]

Parker JG; Zweifel LS; Clark JJ; Evans SB; Phillips PE; Palmiter RD. 2010. Absence of NMDA receptors in dopamine neurons attenuates dopamine release but not conditioned approach during Pavlovian conditioning. Proc Natl Acad Sci U S A 107(30):13491-6. [PubMed: 20616081]  [MGI Ref ID J:162402]

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]

Seeman P; Weinshenker D; Quirion R; Srivastava LK; Bhardwaj SK; Grandy DK; Premont RT; Sotnikova TD; Boksa P; El-Ghundi M; O'dowd BF; George SR; Perreault ML; Mannisto PT; Robinson S; Palmiter RD; Tallerico T. 2005. Dopamine supersensitivity correlates with D2High states, implying many paths to psychosis. Proc Natl Acad Sci U S A 102(9):3513-8. [PubMed: 15716360]  [MGI Ref ID J:96985]

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]

Short JL; Ledent C; Borrelli E; Drago J; Lawrence AJ. 2006. Genetic interdependence of adenosine and dopamine receptors: Evidence from receptor knockout mice. Neuroscience 139(2):661-70. [PubMed: 16476524]  [MGI Ref ID J:107738]

Smith DR; Striplin CD; Geller AM; Mailman RB; Drago J; Lawler CP ; Gallagher M. 1998. Behavioural assessment of mice lacking D1A dopamine receptors. Neuroscience 86(1):135-46. [PubMed: 9692749]  [MGI Ref ID J:48769]

Stanwood GD; Parlaman JP; Levitt P. 2005. Anatomical abnormalities in dopaminoceptive regions of the cerebral cortex of dopamine D1 receptor mutant mice. J Comp Neurol 487(3):270-82. [PubMed: 15892099]  [MGI Ref ID J:99709]

Stanwood GD; Parlaman JP; Levitt P. 2006. Genetic or pharmacological inactivation of the dopamine D1 receptor differentially alters the expression of regulator of G-protein signalling (Rgs) transcripts. Eur J Neurosci 24(3):806-18. [PubMed: 16930410]  [MGI Ref ID J:112924]

Stipanovich A; Valjent E; Matamales M; Nishi A; Ahn JH; Maroteaux M; Bertran-Gonzalez J; Brami-Cherrier K; Enslen H; Corbille AG; Filhol O; Nairn AC; Greengard P; Herve D; Girault JA. 2008. A phosphatase cascade by which rewarding stimuli control nucleosomal response. Nature 453(7197):879-84. [PubMed: 18496528]  [MGI Ref ID J:137074]

Ting-A-Kee R; Mercuriano LE; Vargas-Perez H; George SR; van der Kooy D. 2013. Dopamine D1 receptors are not critical for opiate reward but can mediate opiate memory retrieval in a state-dependent manner. Behav Brain Res 247:174-7. [PubMed: 23538064]  [MGI Ref ID J:197617]

Tomiyama K; McNamara FN; Clifford JJ; Kinsella A; Drago J; Tighe O; Croke DT; Koshikawa N; Waddington JL. 2002. Phenotypic resolution of spontaneous and D1-like agonist-induced orofacial movement topographies in congenic dopamine D1A receptor 'knockout' mice. Neuropharmacology 42(5):644-52. [PubMed: 11985822]  [MGI Ref ID J:97339]

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]

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]

Wong JY; Clifford JJ; Massalas JS; Finkelstein DI; Horne MK; Waddington JL; Drago J. 2003. Neurochemical changes in dopamine D1, D3 and D1/D3 receptor knockout mice. Eur J Pharmacol 472(1-2):39-47. [PubMed: 12860471]  [MGI Ref ID J:103739]

Wong JY; Clifford JJ; Massalas JS; Kinsella A; Waddington JL; Drago J. 2003. Essential conservation of D1 mutant phenotype at the level of individual topographies of behaviour in mice lacking both D1 and D3 dopamine receptors. Psychopharmacology (Berl) 167(2):167-73. [PubMed: 12652349]  [MGI Ref ID J:103886]

Health & husbandry

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.

Health & Colony Maintenance Information

Animal Health Reports

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

Colony Maintenance

Breeding & HusbandryThis strain is maintained by mating homozygous siblings.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3300.00
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 willfulfill 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* $4290.00
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 willfulfill 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
   None Available
 
  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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