Phenotypes associated with this allele
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Scn5atm1Clhh mutation
(0 available);
any
Scn5a mutation
(104 available)
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mortality/aging
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• mice begin to die at E10.5 and none are born
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embryo
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• at E10.5, all embryos exhibit necrosis compared to no wild-type mice
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• at E10.5, 2 of 5 mice are smaller than wild-type
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cardiovascular system
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• at E10.5, 1 of 5 mice exhibited an irregular heartbeat
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growth/size/body
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• at E10.5, 2 of 5 mice are smaller than wild-type
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cellular
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• at E10.5, all embryos exhibit necrosis compared to no wild-type mice
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Allelic Composition |
Scn5atm1Clhh/Scn5a+
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Genetic Background |
involves: 129 * 129S/SvEv * C57BL/6J |
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Scn5atm1Clhh mutation
(0 available);
any
Scn5a mutation
(104 available)
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mortality/aging
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• following tail clipping one mouse exhibited generalized seizure and died
• however, the lifespan of other mice is normal
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• fewer than expected mice are recovered 3 to 4 weeks after birth
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cardiovascular system
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• unlike in wild-type mice, application of programmed electrical stimulation induced ventricular tachycardia in 8 of 9 mice
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• electrogram duration (EGD) during programmed electrical stimulation parallels (PES) arrhythmic tendencies
• unlike in wild-type mice, propranolol fails to suppress arrhythmias following treatment with isoproterenol
• isoproterenol does not affect arrhythmia status during PES whereas in wild-type mice it induces arrhythmic effects
• mexiletine suppresses arrhythmias in 4 of 5 mice without effecting EGD
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• hearts exhibit greater increases in electrogram duration (EGD) than wild-type hearts during programmed electrical stimulation (PES)
• EGD during PES parallels arrhythmic tendencies
• mice exhibit greater stimulus to response latencies measured at the beginning of the PES sequences than do wild-type mice
• mice exhibit larger ventricular effective refractory period than wild-type mice (37+/-7 msec compared to 29+/-6 msec)
• unlike in wild-type mice, 1 uM propranolol accentuates the increase in EGD as S1S2 intervals are shortened
• treatment with propranolol increases EGD
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• action potential is prolonged in myocytes (152+/-17.8 msec compared to 55+/-6.6 msec in wild-type cells)
• unlike in wild-type mice, myocytes exhibit early afterdepolarization and persistent sodium tail currents
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behavior/neurological
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• following tail clipping one mouse exhibited generalized seizure and died
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nervous system
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• following tail clipping one mouse exhibited generalized seizure and died
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Allelic Composition |
Scn5atm1Clhh/Scn5a+
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Genetic Background |
involves: 129/SvEv |
|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Scn5atm1Clhh mutation
(0 available);
any
Scn5a mutation
(104 available)
|
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cardiovascular system
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• 6 of 10 mice under ketamine anesthesia show sinus bradycardia after pacing
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• electrocardiographic waveforms suggest depressed intra-atrial, atrioventricular node, and intraventricular conduction in the absence of sinoatrial exit block
• sinatrial preparations show depressed sinus rate, greater excitation latencies and slowed conduction velocities for the spread of excitation between the sinoatrial node and atrial septum
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• electrocardiographic waveforms suggest slow atrioventricular node conduction
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• 4 of 10 mice under ketamine anesthesia show II to III atrioventricular block
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• mice under avertin anesthesia show longer PR intervals
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• mice under avertin anesthesia show longer QRS durations
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• mice under avertin anesthesia show abnormal ventricular repolarization, seen as increased QT and corrected QT intervals (after correction for RR intervals) compared with wild-type mice
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• mice under ketamine or avertin anesthesia exhibit greater sinus node recovery times after a burst pacing protocol over a 30-second stimulation period, indicating depressed sinoatrial node pacemaker function
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