Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nrcam20884 mutation
(1 available);
any
Nrcam mutation
(87 available)
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behavior/neurological
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• inconsistently significant weakness is detected in the forepaws starting a 14 weeks of age
• however, hindpaw grip strength is normal
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nervous system
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• unlike Nrcam 20884 Lpin120884 double homozygotes no defects in nerve morphology are detected
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• by 8 weeks of age conduction velocity is reduced in the sciatic nerve and the sural nerve
• decrease is less than in Nrcam 20884 Lpin120884 double homozygotes
• by 12 weeks of age nerve conduction in the sciatic nerve but not the sural nerve is similar to wild-type controls
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behavior/neurological
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• hindlimbs become fully paralyzed, although some hip function may be retained
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• forelimbs show partial loss of function
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muscle
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• develop severe muscle wasting by 2.5 weeks of age
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growth/size/body
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• seen by 2.5 weeks of age
• double mutants are considerably smaller than Lpin1 single homozygous littermates
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behavior/neurological
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• at 4 weeks of age hindlimb grip strength is significantly reduced
• at 6 weeks of age half of the mice are unable to grip with their hindpaws
• by 8 weeks of age all of the mice are unable to grip with their hindpaws
• between 32 and 48 weeks of age all mice regain the ability to grip with their hindpaws
• reduced forelimb grip strength is seen at 6 weeks of age, weakness attenuates starting around 24 weeks of age
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• develop a floppy gait by 5 weeks of age
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• develop hindlimb paralysis by 6 to 7 weeks of age
• paralysis is characterized by partial to total loss of hindlimb joint mobility, inability to grip with the hind paws, and hindlimb grasping when suspended by the tail
• paralysis phenotype attenuates over time
• after 14 weeks of age hindlimbs take on a flaccid disposition and progressively regain mobility and strength
• between 8 months and 1 year of age mice regain the ability to grip structures and walk although the gait remains floppy
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• develop hindlimb paralysis by 6 to 7 weeks of age
• paralysis is characterized by partial to total loss of hindlimb joint mobility, inability to grip with the hind paws, and hindlimb grasping when suspended by the tail
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• appear to be incapable of suckling pups
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nervous system
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• at 12 weeks of age some axons in the sciatic nerve have thin myelin sheaths
• at 12 weeks of age compact myelin structures are seen beside axons within Schwann cells
• at 52 weeks of age some axons with thin myelin sheaths are still present but the overall state of myelination has improved
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• at 8 weeks of age demyelinated axons are present and darkly stained debris is seen in the sciatic nerve
• appear less well organized compared to controls
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• at 8 and 12 weeks of age demyelinated axons are present in the sciatic nerve
• at 52 weeks of age some demyelinated axons are still present but the overall state of myelination has improved
• demyelination peaks at 8 weeks of age
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• compound muscle action potentials are reduced at 8 and 12 weeks of age in the sciatic nerve and the sural nerve
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• at 4 and 8 weeks of age conduction velocity is reduced in the sciatic nerve and the sural nerve
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muscle
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• widespread atrophic fibers are seen in the hindquarters of mice with hindlimb paralysis
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skeleton
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• at the onset of paralysis joints appear stiff and are restricted to a bent position
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growth/size/body
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• associated with onset of paralysis and muscle wasting
• body weight recovers in association with attenuation of paralysis and muscle wasting
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Analysis Tools
