JAX Mouse Strain Datasheet - 003143

B6.129-Gria2^tm1Rod/J

Stock No:: 003143 |; GluR2-

Cryo Recovery

Overview

Also Known As: GluR2-

These Gria2 knock-out mice exhibit an increase in Ca²⁺ permeability and enhanced long-term potentiation.

Donating Investigator

IMR Colony, The Jackson Laboratory

Genetic overview

Genetic Background	Generation
000664 C57BL/6J

Gria2^tm1Rod

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Gria2	glutamate receptor, ionotropic, AMPA2 (alpha 2)

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Research Applications

Cell Biology Research
Neurobiology Research

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Base Price

Starting at:

$2,595.00 Domestic price Cryo Recovery

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Details

Detailed 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.

Development

The targeting vector was designed to delete transmembrane region 1 and the pore loop (exon 11), both of which are necessary for receptor function. The 129X1/SvJ x 129S1/Sv-derived R1 ES cell line was used. This strain arrived on a STOCK background (see Stock No. 002913) and was then backcrossed to C57BL/6J to generate this congenic strain.

Control Suggestions

Wild-type from the colony

Additional Information

Considerations for Choosing Controls

Selected References

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: J:64275

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Genetics

Gria2^tm1Rod

Allele Symbol: Gria2^tm1Rod

Allele Name	targeted mutation 1, John Roder
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	GluA2; GluR2-
Gene Symbol and Name	Gria2, glutamate receptor, ionotropic, AMPA2 (alpha 2)
Gene Synonym(s)	GLUR2; GLURB; GluA2; GluR-B; GluR-K2; GluR2; Glur-2; Glur-2; Glur2; Glur2; HBGR2; gluR-B; glutamate receptor 2 (alpha 2)
Strain of Origin	(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Chromosome	3
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.
Mutations Made By	Dr. John Roder, University of Toronto

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Genotype: Gria2^tm1Rod related

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

Mammalian Phenotype Terms by Genotype

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
- higher elevations of the intracellular Ca2+ concentration upon AMPA receptor stimulation
- normal number of AMPA receptors in the cell membrane

increased susceptibility to neuronal excitotoxicity
- increased vulnerability to AMPA receptor-mediated excitotoxicity

homeostasis/metabolism phenotype

increased susceptibility to neuronal excitotoxicity
- increased vulnerability to AMPA receptor-mediated excitotoxicity

cellular phenotype

increased susceptibility to neuronal excitotoxicity
- increased vulnerability to AMPA receptor-mediated excitotoxicity

Genotype: 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
- higher elevations of the intracellular Ca2+ concentration upon AMPA receptor stimulation
- normal number of AMPA receptors in the cell membrane

increased susceptibility to neuronal excitotoxicity
- abolished AMPA receptor-mediated cell death in cultured motor neurons by the external polyamine 1-naphtyl acetyl spermine (NAS)
- increased vulnerability to AMPA receptor-mediated excitotoxicity

behavior/neurological phenotype

abnormal limb posture
- abnormal posturing of both forelimbs and hind limbs during manipulations

abnormal response to novel object
- reduced object exploration

decreased grip strength
- slightly lower grip strength in fore limbs

hypoactivity
- reduced spontaneous activity during the night

impaired coordination
- unable to walk on a rotarod

homeostasis/metabolism phenotype

increased susceptibility to neuronal excitotoxicity
- abolished AMPA receptor-mediated cell death in cultured motor neurons by the external polyamine 1-naphtyl acetyl spermine (NAS)
- increased vulnerability to AMPA receptor-mediated excitotoxicity

cellular phenotype

increased susceptibility to neuronal excitotoxicity
- abolished AMPA receptor-mediated cell death in cultured motor neurons by the external polyamine 1-naphtyl acetyl spermine (NAS)
- increased vulnerability to AMPA receptor-mediated excitotoxicity

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

Genotype: Gria2^tm1Rod/Gria2^tm1Rod
involves: 129S1/Sv * 129X1/SvJ * CD-1

mortality/aging

postnatal lethality, incomplete penetrance
- by 2 - 3 weeks of age about 20% of homozygotes die

behavior/neurological phenotype

abnormal reflex
- impaired eye closure reflex to approaching objects

abnormal response to novel object
- object exploration is reduced

decreased exploration in new environment

decreased grooming behavior

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

nervous system phenotype

enhanced long term potentiation
- LTP in CA1 region of the hippocampus is enhanced 2-fold and non-saturating

growth/size/body region 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

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

References

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: 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: J:68428

Additional - 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: 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: 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: 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: J:146934
Harlow DE; Saul KE; Komuro H; Macklin WB. 2015. Myelin Proteolipid Protein Complexes with alphav Integrin and AMPA Receptors In Vivo and Regulates AMPA-Dependent Oligodendrocyte Progenitor Cell Migration through the Modulation of Cell-Surface GluR2 Expression. J Neurosci 35(34):12018-32. PubMed: 26311781 MGI: J:226168
Herring BE; Shi Y; Suh YH; Zheng CY; Blankenship SM; Roche KW; Nicoll RA. 2013. Cornichon proteins determine the subunit composition of synaptic AMPA receptors. Neuron 77(6):1083-96. PubMed: 23522044 MGI: J:197912
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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: J:131170
Taylor EW; Wang K; Nelson AR; Bredemann TM; Fraser KB; Clinton SM; Puckett R; Marchase RB; Chatham JC; McMahon LL. 2014. O-GlcNAcylation of AMPA receptor GluA2 is associated with a novel form of long-term depression at hippocampal synapses. J Neurosci 34(1):10-21. PubMed: 24381264 MGI: J:205592
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: 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: 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: 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: J:168565

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service	Genotype	Price
	Heterozygous or Wild-type for Gria2<tm1Rod>

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.

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.

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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.

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.

Terms Of Use

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General Terms and Conditions

Questions about Terms of Use

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Licensing Information

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Email: TechTran@jax.org

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Also Known As: GluR2-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Gria2tm1Rod

Allele Symbol: Gria2tm1Rod

Disease Terms

Research Areas By Genotype

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

Genotype: Gria2tm1Rod related

Mammalian Phenotype Terms by Genotype

Genotype: Gria2tm1Rod/Gria2+B6.129-Gria2tm1Rod/J

nervous system phenotype

homeostasis/metabolism phenotype

cellular phenotype

Genotype: Gria2tm1Rod/Gria2tm1RodB6.129-Gria2tm1Rod/J

nervous system phenotype

behavior/neurological phenotype

homeostasis/metabolism phenotype

cellular phenotype

Genotype: Gria2tm1Rod/Gria2tm1Rodinvolves: 129S1/Sv * 129X1/SvJ * CD-1

mortality/aging

behavior/neurological phenotype

nervous system phenotype

growth/size/body region phenotype

References

Additional References

Additional - Gria2tm1Rod related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Progeny testing is not required

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Gria2^tm1Rod

Allele Symbol: Gria2^tm1Rod

Genotype: Gria2^tm1Rod related

Genotype: Gria2^tm1Rod/Gria2⁺
B6.129-Gria2^tm1Rod/J

Genotype: Gria2^tm1Rod/Gria2^tm1Rod
B6.129-Gria2^tm1Rod/J

Genotype: Gria2^tm1Rod/Gria2^tm1Rod
involves: 129S1/Sv * 129X1/SvJ * CD-1

Additional - Gria2^tm1Rod related