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)|
|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.
When using the GluR2- mouse strain in a publication, please cite the originating article(s) and include JAX stock #003143 in your Materials and Methods section.