Analysis Tools|
Allele Symbol Allele Name Allele ID |
Cnr1tm1.2Ltz targeted mutation 1.2, Beat Lutz MGI:3045419 |
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| Summary |
6 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following treatment with an adenoviral cre, kainic acid induces stronger seizures than in wild-type or untreated mice
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• following treatment with an adenoviral cre, kainic acid induces stronger seizures than in wild-type or untreated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 30 mg/kg kainic acid induces stronger seizures than in wild-type mice
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• misrouted thalamocortical axons (TCAs) are observed in mutants but not in controls, similar to the complete Cnr1tm1.1Ltz total null animals at E16.5
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• deficits in fasciculation at E16.5 are similar to those observed in Cnr1tm1.1Ltz total null animals at E16.5
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• 30 mg/kg kainic acid induces stronger seizures than in wild-type mice
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• 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
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• 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
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• deficits in fasciculation at E16.5 are similar to those observed in Cnr1tm1.1Ltz total null animals at E16.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following injections of kainic acid (an excitotoxin) mutant mice carrying the transgene display decreased survival compared to mutant mice not carrying the transgene
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• 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
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• 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
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• 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
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• 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
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• following injections of kainic acid (an excitotoxin) mutant mice carrying the transgene display decreased survival compared to mutant mice not carrying the transgene
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• depolarization-induced suppression of inhibition, as measured by evoked inhibitory postsynaptic current amplitude, is abolished
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| 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• kainic acid induces stronger seizures than in wild-type mice
• however, diazepam protects mice and wild-type mice similarly against kainic acid-induced seizures
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• kainic acid induces stronger seizures than in wild-type mice
• however, diazepam protects mice and wild-type mice similarly against kainic acid-induced seizures
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• 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
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 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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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 11/12/2024 MGI 6.24 |
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