Phenotypes associated with this allele

• Allele Symbol: Nr3c1^tm2.1Ljm
• Allele Name: targeted mutation 2.1, Louis J Muglia
• Allele ID: MGI:4456461
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Nr3c1^tm2.1Ljm/Nr3c1^tm2.1Ljm Lyz2^tm1(cre)Ifo/Lyz2^+	involves: 129P2/OlaHsd * 129S6/SvEvTac	MGI:5803964
cn2	Nr3c1^tm2.1Ljm/Nr3c1^tm2.1Ljm Tg(Camk2a-cre)T29-1Stl/0	involves: 129S6/SvEvTac * BALB/c * C57BL	MGI:5803966

Genotype
MGI:5803964

cn1

• Allelic Composition: Nr3c1^tm2.1Ljm/Nr3c1^tm2.1Ljm; Lyz2^tm1(cre)Ifo/Lyz2⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S6/SvEvTac

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

cellular

decreased susceptibility to neuronal excitotoxicity ( J:197150 )

• with prior treatment with glucocorticoid stress hormone followed by middle cerebral artery occlusion

hematopoietic system

abnormal monocyte cell number ( J:197150 )

• prior to glucocorticoid stress hormone treatments fail to exhibit a reduction in numbers of infiltrating monocytes in infarcted hemisphere unlike in wild-type mice

homeostasis/metabolism

decreased susceptibility to neuronal excitotoxicity ( J:197150 )

• with prior treatment with glucocorticoid stress hormone followed by middle cerebral artery occlusion

abnormal response to CNS ischemic injury ( J:197150 )

• prior treatment with glucocorticoid stress hormone fail to exhibit a reduction in numbers of infiltrating monocytes and IL6 protein levels in infarcted hemisphere after middle cerebral artery occlusion unlike in wild-type mice

immune system

abnormal monocyte cell number ( J:197150 )

• prior to glucocorticoid stress hormone treatments fail to exhibit a reduction in numbers of infiltrating monocytes in infarcted hemisphere unlike in wild-type mice

increased interleukin-1 beta secretion ( J:197150 )

• in the ischemic cortex after middle cerebral artery occlusion

• in the hippocampus 12, but not 72, hours after kainic acid treatment

abnormal interleukin-6 secretion ( J:197150 )

• prior treatment with glucocorticoid stress hormone fails to induce a decrease in IL6 levels in the ischemic cortex 24 h after middle cerebral artery occlusion

nervous system

decreased susceptibility to neuronal excitotoxicity ( J:197150 )

• with prior treatment with glucocorticoid stress hormone followed by middle cerebral artery occlusion

abnormal response to CNS ischemic injury ( J:197150 )

• prior treatment with glucocorticoid stress hormone fail to exhibit a reduction in numbers of infiltrating monocytes and IL6 protein levels in infarcted hemisphere after middle cerebral artery occlusion unlike in wild-type mice

Genotype
MGI:5803966

cn2

• Allelic Composition: Nr3c1^tm2.1Ljm/Nr3c1^tm2.1Ljm; Tg(Camk2a-cre)T29-1Stl/0
• Genetic Background: involves: 129S6/SvEvTac * BALB/c * C57BL

nervous system

nervous system phenotype ( J:197150 )

N • as in wild-type mice, prior treatment with glucocorticoid stress hormone followed by middle cerebral artery occlusion sensitizes neurons to excityotoxicity

abnormal response to CNS ischemic injury ( J:197150 )

• prior treatment with glucocorticoid stress hormone fail to exhibit a reduction in numbers of infiltrating monocytes after middle cerebral artery occlusion unlike in wild-type mice

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:197150 )

N • as in wild-type mice, prior treatment with glucocorticoid stress hormone followed by middle cerebral artery occlusion sensitizes neurons to excityotoxicity

abnormal response to CNS ischemic injury ( J:197150 )

• prior treatment with glucocorticoid stress hormone fail to exhibit a reduction in numbers of infiltrating monocytes after middle cerebral artery occlusion unlike in wild-type mice