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. Species laboratory mouse Background Strain C57BL/6J Donor Strain 129X1 x 129S1 via R1 (+Kitl-SlJ) ES cell line Generation N5 (25-JAN-04) Generation Definitions   Donating Investigator IMR Colony,   The Jackson Laboratory

Description
Mice homozygous for the Gria2^tm1Rod targeted mutation (GluR2-deficient) were originally reported to be about one half the size of their normal littermates by two to three weeks of age, leading to some preweaning mortality. Growth retardation and mortality can be diminished by reducing litter size and eliminating some competition for the mother's milk. By eight weeks of age, homozygotes appear similar in size and weight to their unaffected littermates. Neurons from Gria2-deficient mice exhibit a 9-fold increase in Ca²⁺ permeability and enhanced long-term potentiation (LTP). Antagonists of AMPA and NMDA receptors block all the enhanced LTP seen in homozygous null mice. Changes in pain thresholds, sensitivity to anaesthetics, focal cerebral ischemia, apoptosis of neuronal subpopulations and learning impairments are also observed.

It has been the experience of The Jackson Laboratory that no homozygous animals have been recovered from heterozygous sibling matings.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Control Information

	Control
	Wild-type from the colony
Considerations for Choosing Controls

Related Strains

Strains carrying   Gria2^tm1Rod allele

002913

STOCK Gria2tm1Rod/J

View Strains carrying   Gria2^tm1Rod     (1 strain)

Strains carrying other alleles of Gria2

012615

B6.129-Gria2tm1Rlh/J

View Strains carrying other alleles of Gria2     (1 strain)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

Gria2^tm1Rod/Gria2⁺

        B6.129-Gria2^tm1Rod/J

• nervous system phenotype
• abnormal AMPA-mediated synaptic currents
  • high degree of inhibition by the external polyamine 1-naphtyl acetyl spermine (NAS), a strong inward rectification and a high relative Ca2+ permeability   (MGI Ref ID J:104951)
  • higher elevations of the intracellular Ca2+ concentration upon AMPA receptor stimulation   (MGI Ref ID J:104951)
  • normal number of AMPA receptors in the cell membrane   (MGI Ref ID J:104951)
• increased susceptibility to neuronal excitotoxicity
  • increased vulnerability to AMPA receptor-mediated excitotoxicity   (MGI Ref ID J:104951)
• homeostasis/metabolism phenotype
• increased susceptibility to neuronal excitotoxicity
  • increased vulnerability to AMPA receptor-mediated excitotoxicity   (MGI Ref ID J:104951)
• cellular phenotype
• increased susceptibility to neuronal excitotoxicity
  • increased vulnerability to AMPA receptor-mediated excitotoxicity   (MGI Ref ID J:104951)

Gria2^tm1Rod/Gria2^tm1Rod

        B6.129-Gria2^tm1Rod/J

• nervous system phenotype
• abnormal AMPA-mediated synaptic currents
  • high degree of inhibition by the external NAS, a strong inward rectification and a high relative Ca2+ permeability   (MGI Ref ID J:104951)
  • higher elevations of the intracellular Ca2+ concentration upon AMPA receptor stimulation   (MGI Ref ID J:104951)
  • normal number of AMPA receptors in the cell membrane   (MGI Ref ID J:104951)
• increased susceptibility to neuronal excitotoxicity
  • increased vulnerability to AMPA receptor-mediated excitotoxicity   (MGI Ref ID J:104951)
  • abolished AMPA receptor-mediated cell death in cultured motor neurons by the external polyamine 1-naphtyl acetyl spermine (NAS)   (MGI Ref ID J:104951)
• behavior/neurological phenotype
• abnormal limb posture
  • abnormal posturing of both forelimbs and hind limbs during manipulations   (MGI Ref ID J:104951)
• abnormal response to novel object
  • reduced object exploration   (MGI Ref ID J:104951)
• decreased grip strength
  • slightly lower grip strength in fore limbs   (MGI Ref ID J:104951)
• hypoactivity
  • reduced spontaneous activity during the night   (MGI Ref ID J:104951)
• impaired coordination
  • unable to walk on a rotarod   (MGI Ref ID J:104951)
• homeostasis/metabolism phenotype
• increased susceptibility to neuronal excitotoxicity
  • increased vulnerability to AMPA receptor-mediated excitotoxicity   (MGI Ref ID J:104951)
  • abolished AMPA receptor-mediated cell death in cultured motor neurons by the external polyamine 1-naphtyl acetyl spermine (NAS)   (MGI Ref ID J:104951)
• cellular phenotype
• increased susceptibility to neuronal excitotoxicity
  • increased vulnerability to AMPA receptor-mediated excitotoxicity   (MGI Ref ID J:104951)
  • abolished AMPA receptor-mediated cell death in cultured motor neurons by the external polyamine 1-naphtyl acetyl spermine (NAS)   (MGI Ref ID J:104951)

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Gria2^tm1Rod/Gria2^tm1Rod

        involves: 129S1/Sv * 129X1/SvJ * CD-1

• mortality/aging
• partial postnatal lethality
  • by 2 - 3 weeks of age about 20% of homozygotes die   (MGI Ref ID J:64275)
• behavior/neurological phenotype
• abnormal reflex
  • impaired eye closure reflex to approaching objects   (MGI Ref ID J:64275)
• abnormal response to novel object
  • object exploration is reduced   (MGI Ref ID J:64275)
• decreased exploration in new environment   (MGI Ref ID J:64275)
• decreased grooming behavior   (MGI Ref ID J:64275)
• impaired coordination
  • impaired coordination on rotorod test; however no signs of seizure activity were detected by observation, EEG, or post-mortem pyramidal cell dropout in the hippocampus   (MGI Ref ID J:64275)
• nervous system phenotype
• enhanced long term potentiation
  • LTP in CA1 region of the hippocampus is enhanced 2-fold and non-saturating   (MGI Ref ID J:64275)
• growth/size phenotype
• decreased body size
  • body size is reduced at 2 - 3 weeks of age; however by 6 - 7 weeks, surviving homozygotes were the same size as littermates   (MGI Ref ID J:64275)
• • decreased body weight
    • body weight is reduced at 2 - 3 weeks of age; however by 6 - 7 weeks, surviving homozygotes were the same weight as littermates   (MGI Ref ID J:64275)

View Research Applications

Research Applications

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

Gria2^tm1Rod related

Cell Biology Research
Channel and Transporter Defects

Neurobiology Research
Channel and Transporter Defects
      sodium/potassium
Epilepsy
Receptor Defects
      glutamate receptor: ionotropic

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Gria2tm1Rod
Allele Name		targeted mutation 1, John Roder
Allele Type		Targeted (knock-out)
Common Name(s)		GluA2; GluR2-;
Mutation Made By		Dr. John Roder,   University of Toronto
Strain of Origin		(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
ES Cell Line Name		R1
ES Cell Line Strain		(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Gene Symbol and Name		Gria2, glutamate receptor, ionotropic, AMPA2 (alpha 2)
Chromosome		3
Gene Common Name(s)		GLUR2; GLURB; GluA2; GluR-B; GluR-K2; Glur-2; Glur2; HBGR2; glutamate receptor 2 (alpha 2);
Molecular Note		A neomycin resistance cassette replaced exon 11 of the gene, which encodes the pore loop and transmembrane region, TM1. Western blots of brain plasma membranes from homozygous mutant mice showed no detectable protein for the targeted gene. [MGI Ref ID J:64275]

Genotyping

Genotyping Information

Genotyping Protocols

Gria2^tm1Rod, Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Jia Z; Agopyan N; Miu P; Xiong Z; Henderson J; Gerlai R; Taverna FA; Velumian A; MacDonald J; Carlen P; Abramow-Newerly W; Roder J. 1996. Enhanced LTP in mice deficient in the AMPA receptor GluR2. Neuron 17(5):945-56. [PubMed: 8938126]  [MGI Ref ID J:64275]

Additional References

Hu RQ; Cortez MA; Man HY; Roder J; Jia Z; Wang YT; Snead OC 3rd. 2001. Gamma-hydroxybutyric acid-induced absence seizures in GluR2 null mutant mice. Brain Res 897(1-2):27-35. [PubMed: 11282355]  [MGI Ref ID J:68428]

Gria2^tm1Rod related

Adesnik H; Nicoll RA. 2007. Conservation of glutamate receptor 2-containing AMPA receptors during long-term potentiation. J Neurosci 27(17):4598-602. [PubMed: 17460072]  [MGI Ref ID J:121085]

Biou V; Bhattacharyya S; Malenka RC. 2008. Endocytosis and recycling of AMPA receptors lacking GluR2/3. Proc Natl Acad Sci U S A 105(3):1038-43. [PubMed: 18195348]  [MGI Ref ID J:131171]

Gerlai R; Henderson JT; Roder JC; Jia Z. 1998. Multiple behavioral anomalies in GluR2 mutant mice exhibiting enhanced LTP. Behav Brain Res 95(1):37-45. [PubMed: 9754875]  [MGI Ref ID J:78386]

Gladding CM; Collett VJ; Jia Z; Bashir ZI; Collingridge GL; Molnar E. 2009. Tyrosine dephosphorylation regulates AMPAR internalisation in mGluR-LTD. Mol Cell Neurosci 40(2):267-79. [PubMed: 19063969]  [MGI Ref ID J:146934]

Hu RQ; Cortez MA; Man HY; Roder J; Jia Z; Wang YT; Snead OC 3rd. 2001. Gamma-hydroxybutyric acid-induced absence seizures in GluR2 null mutant mice. Brain Res 897(1-2):27-35. [PubMed: 11282355]  [MGI Ref ID J:68428]

Iihara K; Joo DT; Henderson J; Sattler R; Taverna FA; Lourensen S; Orser BA; Roder JC; Tymianski M. 2001. The influence of glutamate receptor 2 expression on excitotoxicity in Glur2 null mutant mice. J Neurosci 21(7):2224-39. [PubMed: 11264298]  [MGI Ref ID J:68447]

Jackson AC; Nicoll RA. 2011. Stargazin (TARP {gamma}-2) Is Required for Compartment-Specific AMPA Receptor Trafficking and Synaptic Plasticity in Cerebellar Stellate Cells. J Neurosci 31(11):3939-52. [PubMed: 21411637]  [MGI Ref ID J:170457]

Joo DT; Gong D; Sonner JM; Jia Z; MacDonald JF; Eger EI 2nd; Orser BA. 2001. Blockade of AMPA receptors and volatile anesthetics: reduced anesthetic requirements in GluR2 null mutant mice for loss of the righting reflex and antinociception but not minimum alveolar concentration. Anesthesiology 94(3):478-88. [PubMed: 11374610]  [MGI Ref ID J:106294]

Joo DT; Xiong Z; MacDonald JF; Jia Z; Roder J; Sonner J; Orser BA. 1999. Blockade of glutamate receptors and barbiturate anesthesia: increased sensitivity to pentobarbital-induced anesthesia despite reduced inhibition of AMPA receptors in GluR2 null mutant mice [see comments] Anesthesiology 91(5):1329-41. [PubMed: 10551584]  [MGI Ref ID J:59684]

Lu W; Shi Y; Jackson AC; Bjorgan K; During MJ; Sprengel R; Seeburg PH; Nicoll RA. 2009. Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach. Neuron 62(2):254-68. [PubMed: 19409270]  [MGI Ref ID J:155070]

Mainen ZF; Jia Z; Roder J; Malinow R. 1998. Use-dependent AMPA receptor block in mice lacking GluR2 suggests postsynaptic site for LTP expression. Nat Neurosci 1(7):579-86. [PubMed: 10196565]  [MGI Ref ID J:50786]

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. Involvement of AMPA receptor GluR2 subunits in stimulus-reward learning: evidence from glutamate receptor gria2 knock-out mice. J Neurosci 23(29):9500-7. [PubMed: 14573529]  [MGI Ref ID J:86306]

Medvedev NI; Rodriguez-Arellano JJ; Popov VI; Davies HA; Tigaret CM; Schoepfer R; Stewart MG. 2008. The glutamate receptor 2 subunit controls post-synaptic density complexity and spine shape in the dentate gyrus. Eur J Neurosci 27(2):315-25. [PubMed: 18215230]  [MGI Ref ID J:132175]

Meng Y; Zhang Y; Jia Z. 2003. Synaptic transmission and plasticity in the absence of AMPA glutamate receptor GluR2 and GluR3. Neuron 39(1):163-76. [PubMed: 12848940]  [MGI Ref ID J:84336]

Panicker S; Brown K; Nicoll RA. 2008. Synaptic AMPA receptor subunit trafficking is independent of the C terminus in the GluR2-lacking mouse. Proc Natl Acad Sci U S A 105(3):1032-7. [PubMed: 18195349]  [MGI Ref ID J:131170]

Van Damme P; Braeken D; Callewaert G; Robberecht W; Van Den Bosch L. 2005. GluR2 deficiency accelerates motor neuron degeneration in a mouse model of amyotrophic lateral sclerosis. J Neuropathol Exp Neurol 64(7):605-12. [PubMed: 16042312]  [MGI Ref ID J:104951]

Wang S; Jia Z; Roder J; Murphy TH. 2002. AMPA receptor-mediated miniature synaptic calcium transients in GluR2 null mice. J Neurophysiol 88(1):29-40. [PubMed: 12091530]  [MGI Ref ID J:103180]

Yan J; Zhang Y; Jia Z; Taverna FA; McDonald RJ; Muller RU; Roder JC. 2002. Place-cell impairment in glutamate receptor 2 mutant mice. J Neurosci 22(3):RC204. [PubMed: 11826150]  [MGI Ref ID J:75591]

Zhou Z; Hu J; Passafaro M; Xie W; Jia Z. 2011. GluA2 (GluR2) regulates metabotropic glutamate receptor-dependent long-term depression through N-cadherin-dependent and cofilin-mediated actin reorganization. J Neurosci 31(3):819-33. [PubMed: 21248105]  [MGI Ref ID J:168565]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

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

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

General Supply Notes

• Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

	Control
	Wild-type from the colony
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.

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