All Phenotypes Cacna1a<tm3Maag> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Cacna1a^tm3Maag/Cacna1a^tm3Maag	B6.129P2-Cacna1a^tm3Maag	MGI:3836256
hm2	Cacna1a^tm3Maag/Cacna1a^tm3Maag	involves: 129P2/OlaHsd	MGI:5487277
ht3	Cacna1a^tm3Maag/Cacna1a⁺	B6.129P2-Cacna1a^tm3Maag	MGI:3836257
ht4	Cacna1a^tm3Maag/Cacna1a⁺	involves: 129P2/OlaHsd	MGI:5487278

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Neurological deficits after spreading depression in Cacna1a^tm1Maag/Cacna1a^tm1Maag and Cacna1a^tm3Maag/Cacna1a^tm3Maag mice

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:144701 )

• immediately after a seizure that occurs 45 to 75 minutes following a KCl-induced single spreading depression, 2 of 3 mice die due to respiratory arrest unlike similarly treated wild-type mice

behavior/neurological

enhanced behavioral response to xenobiotic ( J:144701 )

• some mice remain unconscious for up to 10 minutes following a single spreading depression induced by KCl unlike wild-type mice

• topical application of 300 mM KCl induces a single spreading depression that causes hemiplegia, leaning, circling, unconsciousness for up to 10 minutes, seizures 45 to 75 minute after treatment, and, in 2 of 3 mice, death due to respiratory arrest unlike in similarly treated wild-type mice

impaired coordination ( J:144701 )

• following a single spreading depression, mice are unable to move along a wire and fall more often than wild-type mice

• induction of multiple spreading depressions with KCl leads to more severe motor deficits than in wild-type mice

• following induction of multiple spreading depressions with KCl, female mice exhibit more severe and longer lasting motor deficits than male mice and unlike in wild-type mice

abnormal posture ( J:144701 )

• a single spreading depression induced by KCl causes hemiplegia with leaning and circling unlike in wild-type mice

hemiplegia ( J:144701 )

• a single spreading depression induced by KCl causes hemiplegia with leaning and circling unlike in wild-type mice

circling ( J:144701 )

• a single spreading depression induced by KCl causes hemiplegia with leaning and circling unlike in wild-type mice

seizures ( J:144701 )

• 45 to 75 minutes following a single spreading depression induced by KCl unlike in simialrly treated wild-type mice

nervous system

seizures ( J:144701 )

• 45 to 75 minutes following a single spreading depression induced by KCl unlike in simialrly treated wild-type mice

abnormal nervous system electrophysiology ( J:144701 )

• following induction with KCl, spreading depression frequency and propagation speed are increased, especially in females, compared to in wild-type mice and Cacna1a^tm1Maag homozygotes

• ovariectomy and cessation of estrous cycling eliminates sex differences

• KCl-induced cortical spreading depressions propagate into the striatum unlike in wild-type mice with greater frequency and shorter latencies than in Cacna1a^tm1Maag homozygotes

• corticaostriatal propagation of KCl-induced cortical spreading depressions is greater in female mice than in male mice

• mice exhibit 1 or more recurrent spreading depressions following brief topical KCl application and extensive washing unlike in wild-type mice

respiratory system

respiratory failure ( J:144701 )

• immediately after a seizure 45 to 75 minutes following a KCl-induced single spreading depression, 2 of 3 mice die due to respiratory arrest unlike similarly treated wild-type mice

homeostasis/metabolism

abnormal physiological response to xenobiotic ( J:144701 )

• KCl-induced cortical spreading depressions propagate into the striatum unlike in wild-type mice with greater frequency and shorter latencies than in Cacna1a^tm1Maag homozygotes

• corticaostriatal propagation of KCl-induced cortical spreading depressions is greater in female mice than in male mice

• mice exhibit 1 or more recurrent spreading depressions following brief topical KCl application and extensive washing unlike in wild-type mice

increased susceptibility to xenobiotic induced morbidity/mortality ( J:144701 )

• immediately after a seizure that occurs 45 to 75 minutes following a KCl-induced single spreading depression, 2 of 3 mice die due to respiratory arrest unlike similarly treated wild-type mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
familial hemiplegic migraine		DOID:0060178		J:144701

Allelic Composition	Cacna1a^tm3Maag/Cacna1a^tm3Maag
Genetic Background	involves: 129P2/OlaHsd

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cacna1a^tm3Maag mutation (0 available); any Cacna1a mutation (115 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

increased susceptibility to ischemic brain injury ( J:193793 )

• mice show increased vulnerability to ischemic stroke, developing an earlier onset of anoxic depolarization and more frequent peri-infarct depolarizations after filament occlusion of the middle cerebral artery associated with rapid expansion of infarct core on diffusion-weighted magnetic resonance imaging and larger perfusion defects on laser speckle flowmetry

• mutants develop larger areas of cerebral blood flow deficit during distal middle cerebral artery occlusion due to increased susceptibility to ischemic depolarizations

• mutant cortical tissue requires a higher cerebral blood flow threshold level for survival compared to wild-type mice

increased cerebral infarct size ( J:193793 )

• transient filament occlusion of the middle cerebral artery for 1 hour produces larger infarcts than in wild-type mice, with more severe cortical, hippocampal, and thalamic involvement

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:193793 )

• mortality rate following filament occlusion of the middle cerebral artery is higher in mutants, reaching 100% within 24 hours after stroke onset

nervous system

increased susceptibility to ischemic brain injury ( J:193793 )

• mutants develop larger areas of cerebral blood flow deficit during distal middle cerebral artery occlusion due to increased susceptibility to ischemic depolarizations

• mutant cortical tissue requires a higher cerebral blood flow threshold level for survival compared to wild-type mice

increased cerebral infarct size ( J:193793 )

• transient filament occlusion of the middle cerebral artery for 1 hour produces larger infarcts than in wild-type mice, with more severe cortical, hippocampal, and thalamic involvement

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
familial hemiplegic migraine		DOID:0060178		J:193793

Allelic Composition	Cacna1a^tm3Maag/Cacna1a⁺
Genetic Background	B6.129P2-Cacna1a^tm3Maag

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cacna1a^tm3Maag mutation (0 available); any Cacna1a mutation (115 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal nervous system electrophysiology ( J:144701 )

• following induction with KCl, spreading depression frequency and propagation speed are increased compared to in wild-type mice but not as much as in homozygotes

• KCl-induced cortical spreading depressions propagate into the striatum unlike in wild-type mice but not as much as in homozygous mice

• mice exhibit 1 or more recurrent spreading depressions following brief topical KCl application and extensive washing unlike in wild-type mice

• however, recovery of cortical evoked potentials after KCl-induced spreading depression is normal

homeostasis/metabolism

abnormal physiological response to xenobiotic ( J:144701 )

• topical application of 300 mM KCl induces a single spreading depression that causes impairments in coordination not observed in wild-type mice that are not as severe as in homozygous mice

• KCl-induced cortical spreading depressions propagate into the striatum unlike in wild-type mice but not as much as in homozygous mice

• mice exhibit 1 or more recurrent spreading depressions following brief topical KCl application and extensive washing unlike in wild-type mice

• however, recovery of cortical evoked potentials after KCl-induced spreading depression is normal

behavior/neurological

enhanced behavioral response to xenobiotic ( J:144701 )

• topical application of 300 mM KCl induces a single spreading depression that causes impairments in coordination not observed in wild-type mice that are not as severe as in homozygous mice

Allelic Composition	Cacna1a^tm3Maag/Cacna1a⁺
Genetic Background	involves: 129P2/OlaHsd

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cacna1a^tm3Maag mutation (0 available); any Cacna1a mutation (115 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

increased susceptibility to ischemic brain injury ( J:193793 )

• mice show increased vulnerability to ischemic stroke, developing an earlier onset of anoxic depolarization after filament occlusion of the middle cerebral artery

increased cerebral infarct size ( J:193793 )

• transient filament occlusion of the middle cerebral artery for 30 minutes produces larger infarcts than in wild-type mice

• females show more striking increases in infarct volume than males

• treatment with the NMDA antagonist MK-801 significantly reduces infarct volume by 45% in mutants compared with only 23% in wild-type mice

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:193793 )

• females exhibit more than 60% mortality between 24 and 96 hours following transient filament occlusion of the cerebral artery for 30 minutes

nervous system

increased susceptibility to ischemic brain injury ( J:193793 )

• mice show increased vulnerability to ischemic stroke, developing an earlier onset of anoxic depolarization after filament occlusion of the middle cerebral artery

increased cerebral infarct size ( J:193793 )

• transient filament occlusion of the middle cerebral artery for 30 minutes produces larger infarcts than in wild-type mice

• females show more striking increases in infarct volume than males

• treatment with the NMDA antagonist MK-801 significantly reduces infarct volume by 45% in mutants compared with only 23% in wild-type mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
familial hemiplegic migraine		DOID:0060178		J:193793

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