Strain Name:

B6N.129-Gria1tm1Rsp/J

Stock Number:

019011

Order this mouse

Availability:

Cryopreserved - Ready for recovery

Use Restrictions Apply, see Terms of Use
GluA1 knockout mice exhibit behavioral, social, and cognitive deficits. They may have applications in studies related to behavioral, social and cognitive abnormalities, hippocampal synaptic transmission/plasticity, and nociception, as well as neuropsychiatric disorders such as schizophrenia and depression/mania.

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.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
GenerationN5pN1
Generation Definitions
 
Donating Investigator Rolf Sprengel,   Max Planck Institute for Medical Res

Description
The GluA1 knockout allele (also called GluA1-, GluR-A-, or A1-lox) has a deletion of the sequences necessary in formation of the glutamate receptor transmembrane domain ion channel pore (exon 11). No GluA1 protein expression is detected from the targeted allele. Homozygous mice are viable and fertile, with behavioral, social, and cognitive deficits. Specifically, homozygotes have profound impairment of several different spatial working memory tasks and selective impairment on short-term recognition memory tasks. Homozygotes show no alterations on spatial reference memory tasks or long-term memory tasks. GluA1-/- mice also have novelty- and stress-induced hyperactivity, and increased anxiety-related responses. Hippocampal CA1 pyramidal neurons from homozygous mice have strongly reduced extrasynaptic AMPA currents and do not show the dendritic distance-dependent scaling of excitatory synaptic strengths seen in wildtype neurons.

Development
A targeting vector was designed to insert a loxP site upstream of exon 11, and a loxP-flanked neo cassette (from ploxpneo3) downstream of exon 11 of the glutamate receptor, ionotropic, AMPA1 [alpha 1] gene (Gria1; GluR-A, GluA1). This loxP::exon11::loxP::neo::loxP construct was electroporated into (129X1/SvJ x 129S1/Sv)F1-Kitl+-derived R1 embryonic stem (ES) cells. Correctly targeted ES cells with the GluR-Aneo allele (also called 3loxP allele) were then transiently transfected with a Cre recombinase-expressing plasmid. The resulting ES cells with the GluR-A- genotype (both exon 11 and neo selection cassette removed; leaving a single loxP site remaining) were injected into recipient blastocysts. Chimeric mice were bred with C57BL/6 mice to establish the mutant colony. The donating investigator reports that GluR-A- mice were subsequently backcrossed to C57BL/6NCrl mice for ten generations prior to sending to The Jackson Laboratory Repository in 2012. Upon arrival, mice were bred to C57BL/6NJ inbred mice (Stock No. 005304) for at least one generation.

Control Information

  Control
   005304 C57BL/6NJ
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Gria1
024420   B6.129(Cg)-Gria1tm4Rlh/J
008892   B6.129-Gria1tm1Rlh/J
012614   B6.129-Gria1tm2Rlh/J
012612   B6.129-Gria1tm5Rlh/J
012613   B6.129-Gria1tm6Rlh/J
024418   B6.129S6-Gria1tm7Rlh/J
019012   B6N.129-Gria1tm2Rsp/J
024422   C57BL/6-Gria1tm3Rlh/J
View Strains carrying other alleles of Gria1     (8 strains)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Gria1tm1Rsp/Gria1tm1Rsp

        B6.129-Gria1tm1Rsp
  • behavior/neurological phenotype
  • abnormal nociception after inflammation
    • increased spontaneous nocifensive responses to intraplantar capsaicin, however exhibit normal spinal nociceptive tail flick reflex in response to noxious heat and hindpaw withdrawal in response to thermal or mechanical stimuli   (MGI Ref ID J:96597)
  • decreased chemical nociceptive threshold
    • reduction in nociceptive responses in phase II of formalin test and a significantly longer duration of nocifensive behaviors during phase I of formalin test   (MGI Ref ID J:96597)
  • increased anxiety-related response
    • in the elevated zero-maze, mutants make fewer open entries   (MGI Ref ID J:167264)
  • nervous system phenotype
  • abnormal spinal cord morphology
    • number of Ca2+-permeable AMPA channels is decreased in laminae of the spinal cord   (MGI Ref ID J:96597)
  • impaired synaptic plasticity
    • loss of acute, short-term nociceptive plasticity in the spinal dorsal horn   (MGI Ref ID J:96597)
  • reduced AMPA-mediated synaptic currents
    • the AMPA/NMDA peak current ratio and current integral ratio are significantly reduced in spinal neurons   (MGI Ref ID J:96597)
    • AMPA channel-mediated peak currents on second-order spinal neurons are significantly reduced   (MGI Ref ID J:96597)
  • integument phenotype
  • abnormal nociception after inflammation
    • increased spontaneous nocifensive responses to intraplantar capsaicin, however exhibit normal spinal nociceptive tail flick reflex in response to noxious heat and hindpaw withdrawal in response to thermal or mechanical stimuli   (MGI Ref ID J:96597)
  • decreased chemical nociceptive threshold
    • reduction in nociceptive responses in phase II of formalin test and a significantly longer duration of nocifensive behaviors during phase I of formalin test   (MGI Ref ID J:96597)

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

Gria1tm1Rsp/Gria1tm1Rsp

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6
  • growth/size/body phenotype
  • decreased body size
    • mice are smaller than wild-type littermates during first postnatal weeks, but size normalizes post-weaning   (MGI Ref ID J:55695)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • pyramidal cells from hippocampal CA1 region have normal dendrites and spines, and normal morphology of excitatory synapses relative to controls   (MGI Ref ID J:55695)
    • dendritic and spontaneous calcium transients are similar in mutants and wild-type mice   (MGI Ref ID J:55695)
    • reduced AMPA-mediated synaptic currents
      • AMPA currents measured in membrane patches from acute brain slices are strongly reduced compared to wild-type   (MGI Ref ID J:55695)
    • reduced long term potentiation
      • in CA1 slices from adult mice, tetanization produces a persistent potentiation of synaptic responses indicated by increased average field EPSP slopes in wild-type, but mutant mice show no LTP (fEPSPs are not different from pretetanic controls   (MGI Ref ID J:55695)
      • in presence of bicuculline, LTP is absent in mutants but tetanized wild-type controls show 140% (control pathway: 100%) LTP   (MGI Ref ID J:55695)
      • paired-pulse facilitation at CA1 excitatory synapses is similar between mutants and controls   (MGI Ref ID J:55695)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • no deficits in spatial learning or spatial memory acquisition are observed in mutants compared to controls   (MGI Ref ID J:55695)
    • abnormal behavioral response to xenobiotic
      • unlike wild-type, mice do not show significant tolerance to the antinociceptive effect of morphine as determined by the thermal tail flick test; repeated doses with increasing doses of morphine that produce tolerance in wild-type to the antinociceptive effects still produce significant nociception in mutants   (MGI Ref ID J:75498)
      • animals display enhanced context-dependent sensitization to D-amphetamine compared to wild-type or Gria1tm1Erk mice   (MGI Ref ID J:75498)
      • decreased behavioral withdrawal response
        • mice show a lower number of naloxone-precipitated behavioral withdrawal symptoms with chronic morphine treatment compared to wild-type littermates   (MGI Ref ID J:75498)
    • abnormal locomotor behavior
      • increased locomotor activity response to morphine injection is greater than wild-type; however baseline values are higher than controls   (MGI Ref ID J:75498)
      • duration of locomotor activity is slightly higher than controls in males kept isolated for 1, 5, or 21 days   (MGI Ref ID J:101930)
      • hyperactivity
        • slightly hyperactive in novel environment   (MGI Ref ID J:75498)
      • increased vertical activity
        • rear frequency and duration are increased compared to controls in male mice isolated for 1, 5, or 21 days   (MGI Ref ID J:101930)
    • abnormal response to new environment
      • mice are slightly hyperactive when placed in a novel cage, but do show habituation upon repeated exposure to novel cages   (MGI Ref ID J:75498)
      • upon repeated exposure, both mutants and wild-type show habituation but mutants still show slight difference in ambulation   (MGI Ref ID J:75498)
      • increased exploration in new environment
        • male mice kept isolated for 1, 5, or 21 days show increased duration of passive exploration of environment compared to wild-type littermates   (MGI Ref ID J:101930)
    • abnormal sexual interaction
      • males exhibit less sniffing of body of females than wild-type males   (MGI Ref ID J:101930)
    • abnormal social investigation
      • frequency and duration of partner exploration are increased in male mice isolated for 1, 5, or 21 days compared to controls   (MGI Ref ID J:101930)
    • decreased aggression towards males
      • in resident-intruder test, individually tested male mice isolated for 1, 5, or 21 days show reduced frequency and duration of consummate and ambivalent aggression towards an intruder in the resident animal's cage   (MGI Ref ID J:101930)
      • after 30 days in isolation, male mutants do not show increased consummate aggression towards other animals when placed together, in contrast to wild-type males which show high levels of aggression towards other males   (MGI Ref ID J:101930)
      • mutants show a greater duration of defensive behavior after 30 days of isolation than wild-type males   (MGI Ref ID J:101930)
      • after pair-housing with a female for 5 days, mutants show no increased aggressive behavior toward an intruder male whereas aggression is higher in wild-type males   (MGI Ref ID J:101930)
    • decreased anxiety-related response
      • in elevated plus-maze tests, mutant show shorter latencies to enter closed to first entry of open arms, decreased freezing and more entries into open arms compared to wild-type littermates   (MGI Ref ID J:101930)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • following morphine injection, both mutant and wild-type mice show similar morphine levels in brain tissue and plasma samples, indicating similar pharmacokinetics between the genotypes   (MGI Ref ID J:75498)
    • after 4 weeks of social isolation, dopamine levels in the brain of males are similar to controls, as are plasma testosterone levels   (MGI Ref ID J:101930)
    • abnormal serotonin level
      • ratio of 5-hydroxyindoleacetic acid to serotonin in hippocampus are lower than in wild-type after 4 weeks of social isolation; in general, ratios are lower in mutant brains, but only significant decrease is detected in hippocampus   (MGI Ref ID J:101930)

Gria1tm1Rsp/Gria1tm1Rsp

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6J
  • behavior/neurological phenotype
  • abnormal emotion/affect behavior
    • in the elevated plus-maze, mutants make more open and center entries and have more center time but less closed time, than wild-type mice   (MGI Ref ID J:167264)
    • lithium treatment partially rescues the elevated maze test phenotype, with mutants making fewer open entries compared to untreated mutants   (MGI Ref ID J:167264)
    • in the light/dark emergence test, mutants make more shelter exits and show more frequent scanning of the shelter than wild-type, although they do not spend more time out of the shelter than wild-type mice, indicating an increase in risk assessment   (MGI Ref ID J:167264)
    • in repeated exposure to elevated plus-maze, mutants make more open entries than wild-type, regardless of trial, and exhibit more open time; mutants make more closed arm entries on trial 2 but not trial 1   (MGI Ref ID J:167264)
    • all these behaviors are indicative of manic-like phenotype   (MGI Ref ID J:167264)

Gria1tm1Rsp/Gria1tm1Rsp

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J
  • behavior/neurological phenotype
  • abnormal emotion/affect behavior
    • in the elevated plus-maze, mutants make more open and center entries and have more center time but less closed time, than wild-type mice   (MGI Ref ID J:167264)
    • mutants exhibit a decrease in immobility compared to wild-type during the first and sometimes second forced swim trials   (MGI Ref ID J:167264)
    • mutants, but not wild-type mice, exhibit a significant increase in immobility by the third forced swim trial, as compared to trial 1   (MGI Ref ID J:167264)
    • mutants show less immobility and increased swimming, but no difference in climbing, in a modified forced swim test compared to wild-type mice on trial 1 but not trial 2   (MGI Ref ID J:167264)
    • mutants, but not wild-type mice, exhibit an increase in immobility and a decrease in swimming from trial 1 to 2 of the modified forced swim test   (MGI Ref ID J:167264)
    • all these behaviors are indicative of manic-like phenotype   (MGI Ref ID J:167264)
    • increased exploration in new environment
      • mutants travel farther than wild-type mice in a novel open field   (MGI Ref ID J:167264)
      • however, movement in a home cage-like environment is no different from wild-type   (MGI Ref ID J:167264)
  • hyperactivity
    • in a novel open field   (MGI Ref ID J:167264)
    • induced hyperactivity
      • injection stress produces a transient increase in activity in mutants compared to a decrease in locomotor activity in wild-type mice   (MGI Ref ID J:167264)
      • restraint stress produces a greater increase in locomotor activity in mutants than in wild-type mice   (MGI Ref ID J:167264)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • corticosterone levels are similar in mutants as in wild-type after a single forced swim trial   (MGI Ref ID J:167264)
View Research Applications

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

Neurobiology Research
Behavioral and Learning Defects
      high anxiety
Channel and Transporter Defects
      calcium: glutamate receptor
Cortical Defects
Neurotransmitter Receptor and Synaptic Vesicle Defects
Receptor Defects
      glutamate receptor: ionotropic

Research Tools
Neurobiology Research

Sensorineural Research
Nociception

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Gria1tm1Rsp
Allele Name targeted mutation 1, Rolf Sprengel
Allele Type Targeted (Null/Knockout)
Common Name(s) GluA1-; GluR-A-; GluR1-; GluRA-;
Strain of Origin(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Gene Symbol and Name Gria1, glutamate receptor, ionotropic, AMPA1 (alpha 1)
Chromosome 11
Gene Common Name(s) 2900051M01Rik; AI853806; GLUH1; GLUR1; GLURA; Glr-1; Glr1; GluA1; GluR-A; Glur-1; Glur1; HBGR1; HIPA1; RIKEN cDNA 2900051M01 gene; expressed sequence AI853806; glutamate receptor 1; glutamate receptor 1 (alpha 1);
General Note Phenotypic Similarity to Human Syndrome: Schizoaffective Disorder (J:167264).
Molecular Note A single loxP site was inserted into intron 10 and a loxP flanked neomycin selection cassette was inserted into exon 11. The loxP-flanked sequences were deleted in ES cells by transient Cre expression prior to the production of chimeric mice. The finalheritable allele contains a single loxP site replacing exon 11 and flanking intronic sequences. Immunohistochemistry experiments confirmed that no detectable protein is expressed from this allele. [MGI Ref ID J:55695]

Genotyping

Genotyping Information

Genotyping Protocols

Gria1tm1Rsp,

SEPARATED MELT



Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Resnik E; McFarland JM; Sprengel R; Sakmann B; Mehta MR. 2012. The Effects of GluA1 Deletion on the Hippocampal Population Code for Position. J Neurosci 32(26):8952-68. [PubMed: 22745495]  [MGI Ref ID J:185645]

Zamanillo D; Sprengel R; Hvalby O; Jensen V; Burnashev N; Rozov A; Kaiser KM; Koster HJ; Borchardt T; Worley P; Lubke J; Frotscher M; Kelly PH; Sommer B; Andersen P; Seeburg PH; Sakmann B. 1999. Importance of AMPA receptors for hippocampal synaptic plasticity but not for spatial learning [see comments] Science 284(5421):1805-11. [PubMed: 10364547]  [MGI Ref ID J:55695]

Additional References

Gria1tm1Rsp related

Aitta-Aho T; Vekovischeva OY; Neuvonen PJ; Korpi ER. 2009. Reduced benzodiazepine tolerance, but increased flumazenil-precipitated withdrawal in AMPA-receptor GluR-A subunit-deficient mice. Pharmacol Biochem Behav 92(2):283-90. [PubMed: 19141300]  [MGI Ref ID J:151038]

Allen K; Gil M; Resnik E; Toader O; Seeburg P; Monyer H. 2014. Impaired path integration and grid cell spatial periodicity in mice lacking GluA1-containing AMPA receptors. J Neurosci 34(18):6245-59. [PubMed: 24790195]  [MGI Ref ID J:210600]

Andrasfalvy BK; Smith MA; Borchardt T; Sprengel R; Magee JC. 2003. Impaired regulation of synaptic strength in hippocampal neurons from GluR1-deficient mice. J Physiol 552(Pt 1):35-45. [PubMed: 12878757]  [MGI Ref ID J:105274]

Antal M; Fukazawa Y; Eordogh M; Muszil D; Molnar E; Itakura M; Takahashi M; Shigemoto R. 2008. Numbers, densities, and colocalization of AMPA- and NMDA-type glutamate receptors at individual synapses in the superficial spinal dorsal horn of rats. J Neurosci 28(39):9692-701. [PubMed: 18815255]  [MGI Ref ID J:143374]

Cowen MS; Schroff KC; Gass P; Sprengel R; Spanagel R. 2003. Neurobehavioral effects of alcohol in AMPA receptor subunit (GluR1) deficient mice. Neuropharmacology 45(3):325-33. [PubMed: 12871650]  [MGI Ref ID J:179573]

Dong Y; Saal D; Thomas M; Faust R; Bonci A; Robinson T; Malenka RC. 2004. Cocaine-induced potentiation of synaptic strength in dopamine neurons: behavioral correlates in GluRA(-/-) mice. Proc Natl Acad Sci U S A 101(39):14282-7. [PubMed: 15375209]  [MGI Ref ID J:93440]

Feyder M; Wiedholz L; Sprengel R; Holmes A. 2007. Impaired associative fear learning in mice with complete loss or haploinsufficiency of AMPA GluR1 receptors. Front Behav Neurosci 1:4. [PubMed: 18958186]  [MGI Ref ID J:180425]

Fitzgerald PJ; Barkus C; Feyder M; Wiedholz LM; Chen YC; Karlsson RM; Machado-Vieira R; Graybeal C; Sharp T; Zarate C; Harvey-White J; Du J; Sprengel R; Gass P; Bannerman D; Holmes A. 2010. Does gene deletion of AMPA GluA1 phenocopy features of schizoaffective disorder? Neurobiol Dis 40(3):608-21. [PubMed: 20699120]  [MGI Ref ID J:167264]

Freudenberg F; Marx V; Mack V; Layer LE; Klugmann M; Seeburg PH; Sprengel R; Celikel T. 2013. GluA1 and its PDZ-interaction: a role in experience-dependent behavioral plasticity in the forced swim test. Neurobiol Dis 52:160-7. [PubMed: 23262314]  [MGI Ref ID J:197650]

Frey MC; Sprengel R; Nevian T. 2009. Activity pattern-dependent long-term potentiation in neocortex and hippocampus of GluA1 (GluR-A) subunit-deficient mice. J Neurosci 29(17):5587-96. [PubMed: 19403825]  [MGI Ref ID J:148254]

Hardingham N; Fox K. 2006. The role of nitric oxide and GluR1 in presynaptic and postsynaptic components of neocortical potentiation. J Neurosci 26(28):7395-404. [PubMed: 16837587]  [MGI Ref ID J:110659]

Hartmann B; Ahmadi S; Heppenstall PA; Lewin GR; Schott C; Borchardt T; Seeburg PH; Zeilhofer HU; Sprengel R; Kuner R. 2004. The AMPA receptor subunits GluR-A and GluR-B reciprocally modulate spinal synaptic plasticity and inflammatory pain. Neuron 44(4):637-50. [PubMed: 15541312]  [MGI Ref ID J:96597]

Hoffman DA; Sprengel R; Sakmann B. 2002. Molecular dissection of hippocampal theta-burst pairing potentiation. Proc Natl Acad Sci U S A 99(11):7740-5. [PubMed: 12032353]  [MGI Ref ID J:76866]

Humeau Y; Reisel D; Johnson AW; Borchardt T; Jensen V; Gebhardt C; Bosch V; Gass P; Bannerman DM; Good MA; Hvalby O; Sprengel R; Luthi A. 2007. A pathway-specific function for different AMPA receptor subunits in amygdala long-term potentiation and fear conditioning. J Neurosci 27(41):10947-56. [PubMed: 17928436]  [MGI Ref ID J:125699]

Jensen V; Kaiser KM; Borchardt T; Adelmann G; Rozov A; Burnashev N; Brix C; Frotscher M; Andersen P; Hvalby O; Sakmann B; Seeburg PH; Sprengel R. 2003. A juvenile form of postsynaptic hippocampal long-term potentiation in mice deficient for the AMPA receptor subunit GluR-A. J Physiol 553(Pt 3):843-56. [PubMed: 14555717]  [MGI Ref ID J:105497]

Johnson AW; Bannerman DM; Rawlins NP; Sprengel R; Good MA. 2005. Impaired outcome-specific devaluation of instrumental responding in mice with a targeted deletion of the AMPA receptor glutamate receptor 1 subunit. J Neurosci 25(9):2359-65. [PubMed: 15745962]  [MGI Ref ID J:98615]

Mack V; Burnashev N; Kaiser KM; Rozov A; Jensen V; Hvalby O; Seeburg PH; Sakmann B; Sprengel R. 2001. Conditional restoration of hippocampal synaptic potentiation in Glur-A-deficient mice. Science 292(5526):2501-4. [PubMed: 11431570]  [MGI Ref ID J:76021]

Mead AN; Brown G; Le Merrer J; Stephens DN. 2005. Effects of deletion of gria1 or gria2 genes encoding glutamatergic AMPA-receptor subunits on place preference conditioning in mice. Psychopharmacology (Berl) 179(1):164-71. [PubMed: 15619119]  [MGI Ref ID J:110154]

Mead AN; Stephens DN. 2003. Selective disruption of stimulus-reward learning in glutamate receptor gria1 knock-out mice. J Neurosci 23(3):1041-8. [PubMed: 12574434]  [MGI Ref ID J:81913]

Morrell CN; Sun H; Ikeda M; Beique JC; Swaim AM; Mason E; Martin TV; Thompson LE; Gozen O; Ampagoomian D; Sprengel R; Rothstein J; Faraday N; Huganir R; Lowenstein CJ. 2008. Glutamate mediates platelet activation through the AMPA receptor. J Exp Med 205(3):575-84. [PubMed: 18283118]  [MGI Ref ID J:133321]

Phillips KG; Hardingham NR; Fox K. 2008. Postsynaptic action potentials are required for nitric-oxide-dependent long-term potentiation in CA1 neurons of adult GluR1 knock-out and wild-type mice. J Neurosci 28(52):14031-41. [PubMed: 19109486]  [MGI Ref ID J:143884]

Procaccini C; Aitta-aho T; Jaako-Movits K; Zharkovsky A; Panhelainen A; Sprengel R; Linden AM; Korpi ER. 2011. Excessive novelty-induced c-Fos expression and altered neurogenesis in the hippocampus of GluA1 knockout mice. Eur J Neurosci 33(1):161-74. [PubMed: 21073553]  [MGI Ref ID J:174467]

Procaccini C; Maksimovic M; Aitta-Aho T; Korpi ER; Linden AM. 2013. Reversal of novelty-induced hyperlocomotion and hippocampal c-Fos expression in GluA1 knockout male mice by the mGluR2/3 agonist LY354740. Neuroscience 250:189-200. [PubMed: 23867766]  [MGI Ref ID J:207045]

Ranson A; Sengpiel F; Fox K. 2013. The role of GluA1 in ocular dominance plasticity in the mouse visual cortex. J Neurosci 33(38):15220-5. [PubMed: 24048851]  [MGI Ref ID J:202597]

Reisel D; Bannerman DM; Schmitt WB; Deacon RM; Flint J; Borchardt T; Seeburg PH; Rawlins JN. 2002. Spatial memory dissociations in mice lacking GluR1. Nat Neurosci 5(9):868-73. [PubMed: 12195431]  [MGI Ref ID J:78706]

Romberg C; Raffel J; Martin L; Sprengel R; Seeburg PH; Rawlins JN; Bannerman DM; Paulsen O. 2009. Induction and expression of GluA1 (GluR-A)-independent LTP in the hippocampus. Eur J Neurosci 29(6):1141-52. [PubMed: 19302150]  [MGI Ref ID J:147114]

Sanderson DJ; Good MA; Skelton K; Sprengel R; Seeburg PH; Rawlins JN; Bannerman DM. 2009. Enhanced long-term and impaired short-term spatial memory in GluA1 AMPA receptor subunit knockout mice: evidence for a dual-process memory model. Learn Mem 16(6):379-86. [PubMed: 19470654]  [MGI Ref ID J:164960]

Schmitt WB; Arianpour R; Deacon RM; Seeburg PH; Sprengel R; Rawlins JN; Bannerman DM. 2004. The role of hippocampal glutamate receptor-A-dependent synaptic plasticity in conditional learning: the importance of spatiotemporal discontiguity. J Neurosci 24(33):7277-82. [PubMed: 15317854]  [MGI Ref ID J:97149]

Schmitt WB; Deacon RM; Seeburg PH; Rawlins JN; Bannerman DM. 2003. A within-subjects, within-task demonstration of intact spatial reference memory and impaired spatial working memory in glutamate receptor-A-deficient mice. J Neurosci 23(9):3953-9. [PubMed: 12736365]  [MGI Ref ID J:83335]

Schmitt WB; Sprengel R; Mack V; Draft RW; Seeburg PH; Deacon RM; Rawlins JN; Bannerman DM. 2005. Restoration of spatial working memory by genetic rescue of GluR-A-deficient mice. Nat Neurosci 8(3):270-2. [PubMed: 15723058]  [MGI Ref ID J:97573]

Selcher JC; Xu W; Hanson JE; Malenka RC; Madison DV. 2012. Glutamate receptor subunit GluA1 is necessary for long-term potentiation and synapse unsilencing, but not long-term depression in mouse hippocampus. Brain Res 1435:8-14. [PubMed: 22197030]  [MGI Ref ID J:181893]

Taylor AM; Niewoehner B; Seeburg PH; Sprengel R; Rawlins JN; Bannerman DM; Sanderson DJ. 2011. Dissociations within short-term memory in GluA1 AMPA receptor subunit knockout mice. Behav Brain Res 224(1):8-14. [PubMed: 21641937]  [MGI Ref ID J:176997]

Vekovischeva OY; Aitta-Aho T; Echenko O; Kankaanpaa A; Seppala T; Honkanen A; Sprengel R; Korpi ER. 2004. Reduced aggression in AMPA-type glutamate receptor GluR-A subunit-deficient mice. Genes Brain Behav 3(5):253-65. [PubMed: 15344919]  [MGI Ref ID J:101930]

Vekovischeva OY; Zamanillo D; Echenko O; Seppala T; Uusi-Oukari M; Honkanen A; Seeburg PH; Sprengel R; Korpi ER. 2001. Morphine-induced dependence and sensitization are altered in mice deficient in AMPA-type glutamate receptor-A subunits. J Neurosci 21(12):4451-9. [PubMed: 11404432]  [MGI Ref ID J:75498]

Watson RF; Abdel-Majid RM; Barnett MW; Willis BS; Katsnelson A; Gillingwater TH; McKnight GS; Kind PC; Neumann PE. 2006. Involvement of protein kinase A in patterning of the mouse somatosensory cortex. J Neurosci 26(20):5393-401. [PubMed: 16707791]  [MGI Ref ID J:108705]

Wiedholz LM; Owens WA; Horton RE; Feyder M; Karlsson RM; Hefner K; Sprengel R; Celikel T; Daws LC; Holmes A. 2008. Mice lacking the AMPA GluR1 receptor exhibit striatal hyperdopaminergia and 'schizophrenia-related' behaviors. Mol Psychiatry 13(6):631-40. [PubMed: 17684498]  [MGI Ref ID J:151069]

Wright N; Glazewski S; Hardingham N; Phillips K; Pervolaraki E; Fox K. 2008. Laminar analysis of the role of GluR1 in experience-dependent and synaptic depression in barrel cortex. Nat Neurosci 11(10):1140-2. [PubMed: 18776896]  [MGI Ref ID J:141146]

Zhang L; Schessl J; Werner M; Bonnemann C; Xiong G; Mojsilovic-Petrovic J; Zhou W; Cohen A; Seeburg P; Misawa H; Jayaram A; Personius K; Hollmann M; Sprengel R; Kalb R. 2008. Role of GluR1 in activity-dependent motor system development. J Neurosci 28(40):9953-68. [PubMed: 18829953]  [MGI Ref ID J:141815]

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 & HusbandryWhen maintaining a live colony, homozygous mice may be bred together.

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* $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
   005304 C57BL/6NJ
 
  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.


(6.8)