JAX Mice Database - (glutamate receptor: ionotropic)

Search Criteria: Research Area is "Neurobiology Research: Receptor Defects (glutamate receptor: ionotropic)"

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
000593	B6 x B6CBCa A^w-J/A-Grid2^Lc T(2;6)7Ca Mitf^Mi-wh/J	Repository-Cryopreserved
	Mice homozygous for the Mitf^Mi spontaneous mutation are characterized by decreased macrophage chemotactic responses, impaired proliferative responses to B cell and T cell mitogens, diminished responses in vitro to T-dependent and T-independent antigens and reduced NK cell activity.
002440	B6 x BALB/cByJ-Grid2^Lc-J/J	Repository-Cryopreserved

003143	B6.129-Gria2^tm1Rod/J	Repository-Cryopreserved
	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 s ..... For more information please see the full descriiption on the strain data sheet
001046	B6CBACa A^w-J/A-Grid2^Lc/J	Repository-Cryopreserved
	Mice heterozygous for the lurcher spontaneous mutation (Grid^Lc) show a characteristic swaying of the hindquarters and a jerky up and down movement. They are identifiable with sureness by their behavior at 12 to 14 days of age. Homozygous mutant micedie shortly after birth but have no visible abnormalities and show severe postnatal loss of Purkinje cells and granule cells. Virtually no Purkinje cells are found in adults and granule cells are reduced to about 10% of normal. The number of neurons in the inferior olivary nucleus falls to about 25% of normal. Other cell populations are normal. The Lc mutation induces apoptotic programmed death of the cerebellar cortical Purkinje cells. Homozygous mutant mice are reproducibly deficient in defined cell populations and thus have been used to study cerebellar function and the distribution of various brain components on cerebellar cells.
000527	C57BL/6J-Grid2^ho-5J/J	Repository-Cryopreserved

000548	DBA/2J-Grid2^ho-4J/J	Repository-Cryopreserved

002913	STOCK Gria2^tm1Rod/J	Repository-Cryopreserved
	Mice homozygous for the Gria2^tm1Rod targeted mutation (GluR2) were originally reported to be about one half the size of their normal littermates by two to three weeks 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. Homozygotes do appear similar in size and weight by eight weeks of age. Neurons lacking Gria2 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. Unpublished data show changes in pain thresholds, sensitivity to anaesthetics, focal cerebral ischemia, apoptosis of neuronal subpopulations and learning impairments. It has been the experience of The Jackson Laboratory that no homozygous animals can be recovered from heterozygous sibling matings.

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