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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Cnr1tm1.1Ltz
targeted mutation 1.1, Beat Lutz
MGI:2182924
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Cnr1tm1.1Ltz/Cnr1tm1.1Ltz B6.129P2-Cnr1tm1.1Ltz MGI:3831872
hm2
Cnr1tm1.1Ltz/Cnr1tm1.1Ltz involves: 129P2/OlaHsd * C57BL/6N MGI:3045437
ht3
Cnr1tm1.1Ltz/Cnr1+ involves: 129P2/OlaHsd * C57BL/6N MGI:3045438


Genotype
MGI:3831872
hm1
Allelic
Composition
Cnr1tm1.1Ltz/Cnr1tm1.1Ltz
Genetic
Background
B6.129P2-Cnr1tm1.1Ltz
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cnr1tm1.1Ltz mutation (0 available); any Cnr1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• thalamocortical projections are tight bundles in the internal capsule and fascicle arrays in the striatum, similar to wild-type brains
• in postnatal brains at P0, P1, P4 and P7, misrouted axons and aberrant fasciculation are observed in the white matter, striatum, and corticostriatal junction
• most thalamocortical axons (TCAs) display a normal innervation path and targeting, but numerous TCAs are misrouted and extend ventrolaterally in the pallial-subpallial boundary (PSPB) before turning dorsomedially into the cortical plate to join with other TCAs
• most corticothalamic axons (CTAs) show normal innervation paths and targeting, but numerous abnormally large CTA fascicles are observed close to the pallial-subpallial boundary at E16.5
• mutants have more thalamocortical axon (TCA) fascicles (greater than 50%) with diameters > 14 um (some are >25 um, while control brains have very few fascicles that are > 20 um in diameter with 50% having diameters < 8 um at E16.5
• density of fascicles is significantly lower than in controls (3.8 per 10000 sq. um); mutants have fewer but larger TCA fascicles in the pallial-subpallial boundary area
• in postnatal mice (p0-P7), abnormally large TCA fascicles are observed; no correction of the developmental phenotype is observed with age
• under high frequency stimulation, long term potentiation is enhanced
• long term depression of inhibitory postsynaptic currents is absent
• however, long term depression under low frequency stimulation is normal
• suppression of GABA-mediated synaptic transmission does not increase paired-pulse facilitation as in wild-type mice

behavior/neurological
N
• mice exhibit normal foot-shock-induced behavioral sensitization, unconditioned freezing to tone, anxiety-related behaviors, and locomotion
• while mice perform normally in a cued conditioning assays, they fail to extinguish the freezing response over time unlike wild-type mice
• mice fail to exhibit extinction of averse memories as in wild-type mice
• mice exhibit reduced exploratory behavior in an elevated plus maze compared to wild-type mice
• however, locomotion in an open field test is normal

cellular
• mutants have more thalamocortical axon (TCA) fascicles (greater than 50%) with diameters > 14 um (some are >25 um, while control brains have very few fascicles that are > 20 um in diameter with 50% having diameters < 8 um at E16.5
• density of fascicles is significantly lower than in controls (3.8 per 10000 sq. um); mutants have fewer but larger TCA fascicles in the pallial-subpallial boundary area
• in postnatal mice (p0-P7), abnormally large TCA fascicles are observed; no correction of the developmental phenotype is observed with age




Genotype
MGI:3045437
hm2
Allelic
Composition
Cnr1tm1.1Ltz/Cnr1tm1.1Ltz
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cnr1tm1.1Ltz mutation (0 available); any Cnr1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• following injections of kainic acid (an excitotoxin) significantly more mutant mice die within 1 hour compared to wild-type mice

behavior/neurological
• following injections of kainic acid (an excitotoxin) mutant mice display more severe seizures compared to wild-type mice

nervous system
• following injections of kainic acid (an excitotoxin) mutant mice display more severe seizures compared to wild-type mice

homeostasis/metabolism
• following injections of kainic acid (an excitotoxin) significantly more mutant mice die within 1 hour compared to wild-type mice




Genotype
MGI:3045438
ht3
Allelic
Composition
Cnr1tm1.1Ltz/Cnr1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cnr1tm1.1Ltz mutation (0 available); any Cnr1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• following injections of kainic acid (an excitotoxin) and a Cnr1 antagonist heterozygous mice display more severe seizures compared to wild-type mice

nervous system
• following injections of kainic acid (an excitotoxin) and a Cnr1 antagonist heterozygous mice display more severe seizures compared to wild-type mice





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last database update
03/13/2019
MGI 6.13
The Jackson Laboratory