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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Cnr1tm1.2Ltz
targeted mutation 1.2, Beat Lutz
MGI:3045419
Summary 6 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Cnr1tm1.2Ltz/Cnr1tm1.2Ltz involves: 129P2/OlaHsd * C57BL/6NCrl MGI:3758332
cn2
Cnr1tm1.2Ltz/Cnr1tm1.2Ltz
Neurod6tm1(cre)Kan/Neurod6+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6NCrl MGI:3758333
cn3
Cnr1tm1.2Ltz/Cnr1tm1.2Ltz
Tg(Camk2a-cre)2Gsc/0
involves: 129P2/OlaHsd * C57BL/6N MGI:3045440
cn4
Cnr1tm1.2Ltz/Cnr1tm1.2Ltz
Tg(dlx5a-cre)1Mekk/?
involves: 129P2/OlaHsd * C57BL/6NCrl * CD-1 MGI:3758334
cn5
Cnr1tm1.2Ltz/Cnr1tm1.2Ltz
Tg(Camk2a-cre)2Gsc/?
involves: 129P2/OlaHsd * C57BL/6NCrl * FVB/N MGI:3758331
cn6
Cnr1tm1.2Ltz/Cnr1tm1.2Ltz
Tg(dlx5a-cre)1Mekk/?
involves: 129P2/OlaHsd * CD-1 MGI:3758337


Genotype
MGI:3758332
cn1
Allelic
Composition
Cnr1tm1.2Ltz/Cnr1tm1.2Ltz
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6NCrl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cnr1tm1.2Ltz mutation (1 available); any Cnr1 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• following treatment with an adenoviral cre, kainic acid induces stronger seizures than in wild-type or untreated mice

behavior/neurological
• following treatment with an adenoviral cre, kainic acid induces stronger seizures than in wild-type or untreated mice




Genotype
MGI:3758333
cn2
Allelic
Composition
Cnr1tm1.2Ltz/Cnr1tm1.2Ltz
Neurod6tm1(cre)Kan/Neurod6+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6NCrl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cnr1tm1.2Ltz mutation (1 available); any Cnr1 mutation (43 available)
Neurod6tm1(cre)Kan mutation (0 available); any Neurod6 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 30 mg/kg kainic acid induces stronger seizures than in wild-type mice
• misrouted thalamocortical axons (TCAs) are observed in mutants but not in controls, similar to the complete Cnr1tm1.1Ltz total null animals at E16.5
• deficits in fasciculation at E16.5 are similar to those observed in Cnr1tm1.1Ltz total null animals at E16.5

behavior/neurological
• 30 mg/kg kainic acid induces stronger seizures than in wild-type mice
• mutants eat less than controls on the first day of a novel palatable food test, however they progressively increase their palatable food consumption over the next 4 days to a similar level as in controls
• mutants display a very limited physical interaction with a novel object, when the palatability component is removed
• mutants take more time to approach and eat novel food on the first exposure compared to wild-type mice, indicating increased behavioral inhibition in the approach of novel palatable food
• mutants exhibit an increase in both the latencies of contact with the novel food item and to displace the novel object

cellular
• deficits in fasciculation at E16.5 are similar to those observed in Cnr1tm1.1Ltz total null animals at E16.5




Genotype
MGI:3045440
cn3
Allelic
Composition
Cnr1tm1.2Ltz/Cnr1tm1.2Ltz
Tg(Camk2a-cre)2Gsc/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cnr1tm1.2Ltz mutation (1 available); any Cnr1 mutation (43 available)
Tg(Camk2a-cre)2Gsc mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• following injections of kainic acid (an excitotoxin) mutant mice carrying the transgene display decreased survival compared to mutant mice not carrying the transgene

behavior/neurological
• following injections of kainic acid (an excitotoxin) mutant mice carrying the transgene display more severe seizures compared to mutant mice not carrying the transgene
• seizure severity did not differ between mutant mice carrying the transgene and null mice homozygous for Cnr1tm1.1Ltz

nervous system
• following injections of kainic acid (an excitotoxin) mutant mice carrying the transgene display more severe seizures compared to mutant mice not carrying the transgene
• seizure severity did not differ between mutant mice carrying the transgene and null mice homozygous for Cnr1tm1.1Ltz
• kainic acid treated mutant mice carrying the transgene have significantly more apoptosis in the CA1 and CA3 regions of the hippocampus compared to mutant mice not carrying the transgene

homeostasis/metabolism
• kainic acid treated mutant mice carrying the transgene have significantly more apoptosis in the CA1 and CA3 regions of the hippocampus compared to mutant mice not carrying the transgene
• following injections of kainic acid (an excitotoxin) mutant mice carrying the transgene display decreased survival compared to mutant mice not carrying the transgene

cellular
• kainic acid treated mutant mice carrying the transgene have significantly more apoptosis in the CA1 and CA3 regions of the hippocampus compared to mutant mice not carrying the transgene




Genotype
MGI:3758334
cn4
Allelic
Composition
Cnr1tm1.2Ltz/Cnr1tm1.2Ltz
Tg(dlx5a-cre)1Mekk/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6NCrl * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cnr1tm1.2Ltz mutation (1 available); any Cnr1 mutation (43 available)
Tg(dlx5a-cre)1Mekk mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• depolarization-induced suppression of inhibition, as measured by evoked inhibitory postsynaptic current amplitude, is abolished

behavior/neurological
N
• 30 mg/kg kainic acid induces similar seizures as in wild-type mice and diazepam protects mice and wild-type mice similarly against kainic acid-induced seizures




Genotype
MGI:3758331
cn5
Allelic
Composition
Cnr1tm1.2Ltz/Cnr1tm1.2Ltz
Tg(Camk2a-cre)2Gsc/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6NCrl * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cnr1tm1.2Ltz mutation (1 available); any Cnr1 mutation (43 available)
Tg(Camk2a-cre)2Gsc mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• kainic acid induces stronger seizures than in wild-type mice
• however, diazepam protects mice and wild-type mice similarly against kainic acid-induced seizures

behavior/neurological
• kainic acid induces stronger seizures than in wild-type mice
• however, diazepam protects mice and wild-type mice similarly against kainic acid-induced seizures
• mutants exhibit a hyperphagic phenotype compared to controls on the first day of a novel palatable food test, and maintain the higher food intake over the course of the experiment
• mutants show high levels of physical interaction with a novel object from the first experimental day even when the palatability component is removed
• mutants do not show any safety behavior towards the novel food and immediately consume the maximal amount, indicating impaired regulation of behavioral inhibition
• mutants exhibit shorter latencies to contact with the novel food item and to displace the novel object




Genotype
MGI:3758337
cn6
Allelic
Composition
Cnr1tm1.2Ltz/Cnr1tm1.2Ltz
Tg(dlx5a-cre)1Mekk/?
Genetic
Background
involves: 129P2/OlaHsd * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cnr1tm1.2Ltz mutation (1 available); any Cnr1 mutation (43 available)
Tg(dlx5a-cre)1Mekk mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• probability that pyramidal cells will receive VGAT+/VGLUT3+ boutons in layer 2/3 of the neocortex is increased
• however, interneuron migration and neurochemical specification are normal





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last database update
04/09/2024
MGI 6.23
The Jackson Laboratory