Phenotypes associated with this allele
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adra2atm1Bkk mutation
(1 available);
any
Adra2a mutation
(23 available)
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adra2atm1Bkk mutation
(1 available);
any
Adra2a mutation
(23 available)
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cardiovascular system
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• resting heart rate more than 180 beats/min greater than normal
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• unlike wild-type controls, administration of the hypotensive agonist, dexmedetomidine, did not reduce blood pressure
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nervous system
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• increased release at high frequency electrical stimulation
• decreased release at low frequency electrical stimulation
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adra2atm1Bkk mutation
(1 available);
any
Adra2a mutation
(23 available)
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behavior/neurological
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• mice treated with epinephrine fail to reduce burst frequency of induced epileptiform activity unlike in control mice
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nervous system
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• mice treated with epinephrine fail to reduce burst frequency of induced epileptiform activity unlike in control mice
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mortality/aging
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• triple homozygous mutant embryos died between E9.5-E11.5
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cardiovascular system
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• at E9.5, triple mutant embryos had a normal heart rate and a normal cardiac structure
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• at E10.5, only moribund triple mutant embryos displayed bradycardia
• also, triple mutant embryos had normal concentrations of L-dopa and noradrenaline but exhibited a reduction in basal phosphorylation of mitogen activated protein kinase-1 and -3
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embryo
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• the yolk sac of triple homozygous mutant embryos was less vascularized and appeared more translucent relative to wild-type
• the endothelial cells in the yolk sac were often detached from the visceral endoderm cell layer
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• triple mutant mice displayed a significantly reduced density of fetal blood vessels in the placental vascular labyrinth, which leads to embryonic lethality as a result of limited oxygen and nutrient supply
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cardiovascular system
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• double homozygous mutant mice displayed increased plasma noradrenaline concentrations and developed cardiac hypertrophy with reduced left ventricular contractility by 4 months of age
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nervous system
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• the inhibitory effect of brimonidine on norepinephrine release was completely abolished in double homozygous mutant mice
• additional experiments in double homozygous mutant mice demonstrated that ADRA2A inhibits transmitter release at high stimulation frequencies, whereas ADRA2C regulates release at lower levels; both subtypes are, however, required for normal presynaptic control of neurotransmitter release from sympathetic nerves in the heart and from central noradrenergic neurons
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growth/size/body
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• double homozygous mutant mice displayed increased plasma noradrenaline concentrations and developed cardiac hypertrophy with reduced left ventricular contractility by 4 months of age
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