Mice homozygous for the Gria2tm1Rod 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.
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.
|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<+>|
|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
When maintaining a live colony, heterozygous mice may be bred with wildtype siblings or to C57BL/6J inbred mice. In our colonies at The Jackson Laboratory, no homozygous offspring are produced from heterozygous breedings. The expected coat color from breeding is black.
|Please inquire about possible genotypes.|
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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