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Description
Strain Information
Former Names B6C3Fe-a/a-Cacng2stg/+ (Changed: 15-DEC-04 ) Type Mutant Strain; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Mating System Outcross-Intercross (Female x Male) 01-MAR-06 TJL Breeding Summary: homozygote x B6C3Fe a/a F1 then heterozygote x heterozygote Species laboratory mouse Generation N43F1 (13-NOV-08) Appearance
black, ataxic
Related Genotype: a/a Cacng2stg/Cacng2stg
black, unaffected
Related Genotype: a/a ?/+ or a/a Cacng2stg/+Description
Mice homozygous for the spontaneous mutation stargazer (Cacng2stg) are first recognizable at 14 days of age by their smaller body size and slightly ataxic gait. Female stargazer homozygous mutant mice are fertile, but most of the males are unable to breed. The mutation is named for the abnormal head movements resembling choreiform head tossing that is characteristic of these mice. The behavioral symptoms progressively worsen with age, but both males and females will live to over one year of age. Electrocorticographical recordings of stargazer mice reveal frequent, prolonged, generalized spike-wave cortical discharges with behavioral arrest. The abnormal brain wave patterns are similar to those seen in human beings with absence epilepsy. Waggler homozygotes (Cacng2stg-wag) manifest a less severe phenotype than stargazer homozygotes, but do display an ataxic gait and occasional seizures. In general, young stargazer mice are more healthy than waggler homozygotes, but if wagglers reach weaning age, they will usually live for 1 to 2 years. Homozygous waggler males and females will breed, and they display no gross neuroanatomical or histopathologic lesions.Development
Stargazer (Cacng2stg) arose spontaneously in strain A/J at the Jackson Laboratory in 1979. It was carried to N3F1 on the A/J strain and then outcrossed to a B6C3Fe-a/a F1 and continued on that background using the cross intercross system. It was cryopreserved in 1990 by mating heterozygotes at N20. The line that remained on the shelf readhed N40 in 2005.
Control Information
| Control | ||
|---|---|---|
| Untyped from the colony | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying a allele
View Strains carrying a (104 strains)
008624 B6.C-Cacng2stg-3J/LetJ 001883 B6.MRL-Cacng2stg-wag/J
Additional Web Information
JAX® NOTES, Spring 2005, 497. Supression of Absence Epilepsy Seizures Dependent on Complex Balance of Proteins.
Phenotype
Phenotype Information
assigned by genotype
Cacng2stg/Cacng2stg
B6C3Fe a/a-Cacng2stg/J
- behavior/neurological phenotype
- decreased startle reflex (MGI Ref ID J:91987)
- mutants lack the acoustic startle reflex (ASR), but startle reflex to somatic sensory stimuli such as air puffs is intact
- decreased vertical activity (MGI Ref ID J:91987)
- hyperactivity (MGI Ref ID J:91987)
- in photocell activity chambers, mutants display 3-4-fold higher activity compared to control mice while vestibular toxin-treated controls have 10-fold increased activity
- impaired coordination (MGI Ref ID J:91987)
- mutants can only stay on the grid for 60 seconds, coinciding with the turn to 90 degrees, in a cling test; control mice can hang on to the grid for ~180 seconds, including complete inversion of the grid
- in the rotarod test, mutants and drug-treated control mice fall off the rod immediately, often before it begins to move, whereas normal controls can walk for ~the full 5 minute test period
- impaired righting response (MGI Ref ID J:91987)
- when mice are dropped supine from height of 50 cm, mutants show poor air-righting performance, whereas control mice land on their feet ~100% of the time and toxin-treated normal controls land feet-first on ~50% of tests
- when placed inside a tube and inverted to supine position, mutants remain inverted for duration (60 s) of test whereas controls right themselves within a few seconds
- after 30 minutes of intermittent horizontal rotation, control mice display a significant decrease in spontaneous movement, but mutants do not show a decrease
- impaired swimming (MGI Ref ID J:91987)
- mutants cannot keep their heads above water during swimming and rapidly begin a spiraling motion underwater and drown if not rescued
- stereotypic behavior (MGI Ref ID J:91987)
- stereotypic behaviors like circling or abnormal head movements, are evident in all mutants at 2-3 weeks of age, and persist throughout observation period (>1 year)
- circling (MGI Ref ID J:91987)
- in open field test, mice exhibit circling to the left or right; controls do not while in vestibular toxin-treated normal controls, circling is exacerbated compared to mutants
- head bobbing (MGI Ref ID J:91987)
- in open field tests, mutants display rapid vertical bobbing head movements
- head shaking (MGI Ref ID J:91987)
- mice show rapid sideways wagging movements of the head during open field tests
- head tossing (MGI Ref ID J:91987)
- mice show occasional episodes of exaggerated and sustained, elevation of the head, resembling retrocollis, during open field observations
- hearing/vestibular/ear phenotype
- abnormal brainstem auditory evoked potential (MGI Ref ID J:91987)
- ABR thresholds for click as a stimulus are normal, with a trend toward increased thresholds for 8 and 16 kHz tone stimuli in mutants (not reaching significance, though)
- abnormal crista ampullaris morphology (MGI Ref ID J:91987)
- crista show a reduction density of hair cells compared to controls
- abnormal vestibular hair cell morphology (MGI Ref ID J:91987)
- vacuole-like defects measuring 15-25 um are seen in the vestibular epithelium
- cells are disorganized in sensory epithelium; some supporting cell nuclei lose contact with the basement membrane and occupy locations higher in the epithelium
- abnormal type I vestibular cell (MGI Ref ID J:91987)
- afferent nerve calyces surrounding type I hair cells lack the fullness and rich mitochondrial content seen in controls; large vacuole-like defects appear to be localized inside afferent calyces
- these vacuoles are surrounded by normal but small and crowded mitochondria and contain scanty debris like cytosol or mitochondria
- circling (MGI Ref ID J:91987)
- in open field test, mice exhibit circling to the left or right; controls do not while in vestibular toxin-treated normal controls, circling is exacerbated compared to mutants
- decreased startle reflex (MGI Ref ID J:91987)
- mutants lack the acoustic startle reflex (ASR), but startle reflex to somatic sensory stimuli such as air puffs is intact
- head bobbing (MGI Ref ID J:91987)
- in open field tests, mutants display rapid vertical bobbing head movements
- head shaking (MGI Ref ID J:91987)
- mice show rapid sideways wagging movements of the head during open field tests
- head tossing (MGI Ref ID J:91987)
- mice show occasional episodes of exaggerated and sustained, elevation of the head, resembling retrocollis, during open field observations
- nervous system phenotype
- abnormal CNS synapse formation (MGI Ref ID J:116541)
- synaptic size appears smaller
- decreased CNS synapse formation (MGI Ref ID J:116541)
- mutants have lower synaptic density in the cerebellar cortex; there are 25% fewer synapses compared to wild-type
- abnormal Purkinje cell innervation (MGI Ref ID J:116541)
- there are more parallel fiber- Purkinje spine synapses with smaller presynsaptic terminal compared to the postsynaptic spine
- there is a 43% reduction in the mean area of the presynaptic terminals in mutants
- synaptic profile in wild-type shows >80% of synapses having larger parallel fiber varicosities than postsynaptic Purkinje cell spines, while in mutants there is ~equal distribution of synapses with larger parallel fiber area than postsynaptic Purkinje cell spine, those with equal pre- and postsynaptic areas, or with smaller parallel fiber varicosity than the postsynaptic Purkinje cell spine
- abnormal brain wave pattern (MGI Ref ID J:91987)
- saline-treated mutants display frequent abnormal polyspike discharges in the EEG; however, these do not correlate temporally with dyskinetic behaviors
- after nifedipine treatment, polyspike discharges are increased while reducing dyskinesia scores in mutants; an inverse relationship is observed
- abnormal synaptic vesicle morphology (MGI Ref ID J:116541)
- presynaptic vesicles are less dense compared to wild-type
- abnormal synaptic vesicle number (MGI Ref ID J:116541)
- presynaptic vesicles are reduced in number
- there are fewer docked vesicles and fewer vesicles adjacent to the active zone ready to dock in mutants than in wild-type
- abnormal vestibular hair cell morphology (MGI Ref ID J:91987)
- vacuole-like defects measuring 15-25 um are seen in the vestibular epithelium
- cells are disorganized in sensory epithelium; some supporting cell nuclei lose contact with the basement membrane and occupy locations higher in the epithelium
- abnormal type I vestibular cell (MGI Ref ID J:91987)
- afferent nerve calyces surrounding type I hair cells lack the fullness and rich mitochondrial content seen in controls; large vacuole-like defects appear to be localized inside afferent calyces
- these vacuoles are surrounded by normal but small and crowded mitochondria and contain scanty debris like cytosol or mitochondria
Cacng2stg/Cacng2stg
B6C3Fe a/a-Cacng2stg
- growth/size phenotype
- decreased body size (MGI Ref ID J:11008)
- at 14 days, mutants are smaller than wild-type littermates
- behavior/neurological phenotype
- absence seizures (MGI Ref ID J:15527)
- adults exhibit spontaneous spike-wave seizures; seizures do not appear to increase in mean duration or mean incidence with age
- ataxia (MGI Ref ID J:11008)
- homozygotes can be identified at 14 days by mildly ataxic gait
- males are usually more severely affected than females
- head tossing (MGI Ref ID J:11008)
- at 1 month of age, mice display abnormal head movements both at rest and during activity; frequency of movements increase progressively with age
- movement resembles choreiform head tossing; mice elevate heads vertically and maintain an upward gaze for several seconds
- males are usually more severely affected than females
- impaired swimming (MGI Ref ID J:11008)
- mice show severe disturbances in righting reflex during swimming, with wild underwater tumbling motions
- nervous system phenotype
- abnormal CNS synapse formation (MGI Ref ID J:15527)
- the ectopic terminals that are seen do not appear to form synapses with dendrites of basket or granule cells
- abnormal brain wave pattern (MGI Ref ID J:11008)
- electrocorticographic (ECoG) recordings from young adults display prolonged high-amplitue (500uV-1mV), bilaterally symmetrical discharges from neocortex, accompanied by behavioral immobility for the duration of the discharge
- paroxysmal spike bursts show 6-7 spikes/second frequencies, with discharge durations of 1-66 seconds; mean rate or discharge activity is 125/hr
- adults show highly reproducible pattern of spontaneous bilaterally symmetrical 6-7/second spike-wave discharges in cortical and hippocampal regions
- seizure rate ranges from 43-209 discharges/hour with durations ranging from 1-66 seconds with a mean of 4-6 seconds
- patterned spike-wave synchronous discharges represent ~20% of total EEG activity in adult mice
- no spike-wave discharges are recorded in P15 mice but are always present by P18; discharges in immature animals can display slightly slower spike frequency (4-5/sec) but are identical to those seen in adults
- abnormal hippocampal mossy fiber morphology (MGI Ref ID J:15527)
- abnormal innervation (MGI Ref ID J:15527)
- mutants show dense mossy fiber staining along the full extent of the dentate gyrus inner molecular layer whereas wild-type show no staining; this is consistently observed in mutants compared to wild-type
- a 48% increase in density of staining is seen within the inner molecular layer-granular cell layer of adult mutants
- no mossy fiber sprouting is observed prior to seizure onset (at P15), but progressively increasing staining specific for mossy fibers is observed from P30-6 months of age
- abnormal neurogenesis (MGI Ref ID J:15527)
- sprouting of mossy fibers in inner molecular layer and granular cell layer of dentate gyrus increases in mutants compared to wild-type
- absence seizures (MGI Ref ID J:15527)
- adults exhibit spontaneous spike-wave seizures; seizures do not appear to increase in mean duration or mean incidence with age
- loss of hippocampal neurons (MGI Ref ID J:15527)
- neuronal density of hilar neurons in hippocampus is reduced by 16% in adult mutants compared to wild-type; this difference only becomes apparent after onset of seizure activity (P17<)
- reproductive system phenotype
- male infertility (MGI Ref ID J:11008)
- males are infertile
- hearing/vestibular/ear phenotype
- head tossing (MGI Ref ID J:11008)
- at 1 month of age, mice display abnormal head movements both at rest and during activity; frequency of movements increase progressively with age
- movement resembles choreiform head tossing; mice elevate heads vertically and maintain an upward gaze for several seconds
- males are usually more severely affected than females
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Cacng2stg/Cacng2stg
involves: A/J * C3HeB/FeJ * C57BL/6J
- nervous system phenotype
- *normal* nervous system phenotype (MGI Ref ID J:121463)
- synaptic electrophysiology including neurotransmitter release and end plate potentials, as well as responses to channel inhibitors is not different from wild-type NMJs
- abnormal CNS synaptic transmission (MGI Ref ID J:106959)
- peak current densities of low voltage-activated (LVA) calcium channels in thalamocortical neurons at membrane potential of -50 mV are increased by 45% compared to control
- peak current densities of high voltage calcium channels (HVA) in TC neurons are increased compared to wild-type
- abnormal motor neuron morphology (MGI Ref ID J:121463)
- fiber diameter at diaphragm NMJs (14.2 um) is slightly reduced compared with wild-type (15.8 um)
- abnormal neuromuscular synapse morphology (MGI Ref ID J:121463)
- neuromuscular junction area (area staining for acetylcholine receptors) in ~25% smaller relative to wild-type mice (333 um2 vs 446 um2)
Cacng2stg/Cacng2stg
involves: A/J
- behavior/neurological phenotype
- ataxia (MGI Ref ID J:138791)
- growth/size phenotype
- decreased body weight (MGI Ref ID J:138791)
- about 75% the weight of control littermates at P14
Cacng2stg/Cacng2stg
Background Not Specified
- nervous system phenotype
- abnormal AMPA-mediated synaptic currents (MGI Ref ID J:140010)
- AMPAR mediated miniature excitatory post synaptic currents (mEPSC) in inhibitory nucleus reticularis (nRT) neurons are significantly reduced in frequency and amplitude in P14-17 mice
- amplitude, but not frequency, is decreased in older P21-23 mice although there are fewer events
- AMPAR mediated EPSCs frequency and amplitude are not significantly altered in excitatory relay neurons, with the exception that frequency is decreased in older mice
- ratio of AMPA to NMDA EPSCs is reduced by 50% in nRT neurons
- Purkinje cell climbing and parallel fiber synapses both exhibit a decrease in the ratio of stimulation intensity in AMPA to kainite receptor and mGlur-induced EPSCs(70% and 50% respectively)
This mouse can be used to support research in many areas including:Cacng2stg related
Cell Biology Research
Channel and Transporter Defects
calcium
Neurobiology Research
Ataxia (Movement) Defects
Cerebellar Defects
Channel and Transporter Defects
calcium
Epilepsy
Vestibular and Hearing Defects
Sensorineural Research
Vestibular and Hearing Defects
Genes & Alleles
Gene & Allele Information
| Allele Symbol | Cacng2stg | ||
|---|---|---|---|
| Allele Name | stargazer | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | gamma2stg; stg; | ||
| Strain of Origin | A/J | ||
| Gene Symbol and Name | Cacng2, calcium channel, voltage-dependent, gamma subunit 2 | ||
| Chromosome | 15 | ||
| Gene Common Name(s) | AW060990; B230105C07Rik; B930041E13Rik; Ipr328; MGC138502; MGC138504; RIKEN cDNA B230105C07 gene; RIKEN cDNA B930041E13 gene; TARP gamma 2; expressed sequence AW060990; stargazer; stargazin; stg; wag; waggler; | ||
| Molecular Note | The phenotype of the stargazer mouse has been attributed to an early transposon (ETn) insertion into intron 2 of the Cacng2 gene. RT-PCR analysis demonstrated that in addition to aberrant transcripts generated by the insertion, some normally spliced mRNA was detected, suggesting that this mutation does not represent a complete null allele. [MGI Ref ID J:48966] | ||
| Allele Symbol | a | ||
| Allele Name | nonagouti | ||
| Allele Type | Spontaneous | ||
Genotyping
Genotyping Information
Genotyping Protocols
Cacng2stg, Separated PCR
Helpful Links
Genotyping resources and troubleshooting
References
References
Selected Reference(s)
Letts VA; Felix R; Biddlecome GH; Arikkath J; Mahaffey CL; Valenzuela A ; Bartlett FS 2nd ; Mori Y ; Campbell KP ; Frankel WN. 1998. The mouse stargazer gene encodes a neuronal Ca2+-channel gamma subunit [see comments] Nat Genet 19(4):340-7. [PubMed: 9697694] [MGI Ref ID J:48966]
Noebels JL; Qiao X; Bronson RT; Spencer C; Davisson MT. 1990. Stargazer: a new neurological mutant on chromosome 15 in the mouse with prolonged cortical seizures [published erratum appears in Epilepsy Res 1992 Mar;11(1):72] Epilepsy Res 7(2):129-35. [PubMed: 2289471] [MGI Ref ID J:11008]
Additional References
Khan Z; Carey J; Park HJ; Lehar M; Lasker D; Jinnah HA. 2004. Abnormal motor behavior and vestibular dysfunction in the stargazer mouse mutant. Neuroscience 127(3):785-96. [PubMed: 15283975] [MGI Ref ID J:91987]
Letts VA; Valenzuela A; Kirley JP; Sweet HO; Davisson MT; Frankel WN. 1997. Genetic and physical maps of the stargazer locus on mouse chromosome 15. Genomics 43(1):62-8. [PubMed: 9226373] [MGI Ref ID J:38767]
Cacng2stg relatedAizawa M; Ito Y; Fukuda H. 1997. Pharmacological profiles of generalized absence seizures in lethargic, stargazer and gamma-hydroxybutyrate-treated model mice. Neurosci Res 29(1):17-25. [PubMed: 9293489] [MGI Ref ID J:43226]
Ayata C; Shimizu-Sasamata M; Lo EH; Noebels JL; Moskowitz MA. 2000. Impaired neurotransmitter release and elevated threshold for cortical spreading depression in mice with mutations in the alpha1A subunit of P/Q type calcium channels Neuroscience 95(3):639-45. [PubMed: 10670432] [MGI Ref ID J:60492]
Chen L; Chetkovich DM; Petralia RS; Sweeney NT; Kawasaki Y; Wenthold RJ; Bredt DS; Nicoll RA. 2000. Stargazing regulates synaptic targeting of AMPA receptors by two distinct mechanisms. Nature 408(6815):936-43. [PubMed: 11140673] [MGI Ref ID J:66410]
Cho CH; St-Gelais F; Zhang W; Tomita S; Howe JR. 2007. Two families of TARP isoforms that have distinct effects on the kinetic properties of AMPA receptors and synaptic currents. Neuron 55(6):890-904. [PubMed: 17880893] [MGI Ref ID J:132139]
Di Pasquale E; Keegan KD; Noebels JL. 1997. Increased excitability and inward rectification in layer V cortical pyramidal neurons in the epileptic mutant mouse Stargazer. J Neurophysiol 77(2):621-31. [PubMed: 9065835] [MGI Ref ID J:40687]
Hashimoto K; Fukaya M; Qiao X; Sakimura K; Watanabe M; Kano M. 1999. Impairment of AMPA receptor function in cerebellar granule cells of ataxic mutant mouse stargazer. J Neurosci 19(14):6027-36. [PubMed: 10407040] [MGI Ref ID J:56282]
Kaja S; Todorov B; van de Ven RC; Ferrari MD; Frants RR; van den Maagdenberg AM; Plomp JJ. 2007. Redundancy of Cav2.1 channel accessory subunits in transmitter release at the mouse neuromuscular junction. Brain Res 1143:92-101. [PubMed: 17320843] [MGI Ref ID J:121463]
Khan Z; Carey J; Park HJ; Lehar M; Lasker D; Jinnah HA. 2004. Abnormal motor behavior and vestibular dysfunction in the stargazer mouse mutant. Neuroscience 127(3):785-96. [PubMed: 15283975] [MGI Ref ID J:91987]
Letts VA; Kang MG; Mahaffey CL; Beyer B; Tenbrink H; Campbell KP; Frankel WN. 2003. Phenotypic heterogeneity in the stargazin allelic series. Mamm Genome 14(8):506-13. [PubMed: 12925883] [MGI Ref ID J:84624]
Letts VA; Mahaffey CL; Beyer B; Frankel WN. 2005. A targeted mutation in Cacng4 exacerbates spike-wave seizures in stargazer (Cacng2) mice. Proc Natl Acad Sci U S A 102(6):2123-8. [PubMed: 15677329] [MGI Ref ID J:96506]
Meng H; Gao R; Dai Q; Qiao X. 2007. Differential regulation of glutamate receptor-mediated BDNF mRNA expression in the cerebellum and its defects in stargazer mice. Neuropharmacology 53(1):81-91. [PubMed: 17544459] [MGI Ref ID J:129857]
Meng H; Larson SK; Gao R; Qiao X. 2007. BDNF transgene improves ataxic and motor behaviors in stargazer mice. Brain Res 1160:47-57. [PubMed: 17588548] [MGI Ref ID J:123328]
Meng H; Walker N; Su Y; Qiao X. 2006. Stargazin mutation impairs cerebellar synaptogenesis, synaptic maturation and synaptic protein distribution. Brain Res 1124(1):197-207. [PubMed: 17070505] [MGI Ref ID J:116541]
Menuz K; Nicoll RA. 2008. Loss of inhibitory neuron AMPA receptors contributes to ataxia and epilepsy in stargazer mice. J Neurosci 28(42):10599-603. [PubMed: 18923036] [MGI Ref ID J:140010]
Menuz K; O'Brien JL; Karmizadegan S; Bredt DS; Nicoll RA. 2008. TARP redundancy is critical for maintaining AMPA receptor function. J Neurosci 28(35):8740-6. [PubMed: 18753375] [MGI Ref ID J:138791]
Milstein AD; Nicoll RA. 2009. TARP modulation of synaptic AMPA receptor trafficking and gating depends on multiple intracellular domains. Proc Natl Acad Sci U S A 106(27):11348-51. [PubMed: 19549880] [MGI Ref ID J:150819]
Nahm WK; Noebels JL. 1998. Nonobligate role of early or sustained expression of immediate-early gene proteins c-fos, c-jun, and Zif/268 in hippocampal mossy fiber sprouting. J Neurosci 18(22):9245-55. [PubMed: 9801364] [MGI Ref ID J:106958]
Payne HL; Connelly WM; Ives JH; Lehner R; Furtmuller B; Sieghart W; Tiwari P; Lucocq JM; Lees G; Thompson CL. 2007. GABAA {alpha}6-Containing Receptors Are Selectively Compromised in Cerebellar Granule Cells of the Ataxic Mouse, Stargazer. J Biol Chem 282(40):29130-43. [PubMed: 17646167] [MGI Ref ID J:125350]
Payne HL; Donoghue PS; Connelly WM; Hinterreiter S; Tiwari P; Ives JH; Hann V; Sieghart W; Lees G; Thompson CL. 2006. Aberrant GABA(A) receptor expression in the dentate gyrus of the epileptic mutant mouse stargazer. J Neurosci 26(33):8600-8. [PubMed: 16914686] [MGI Ref ID J:111655]
Qiao X; Chen L; Gao H; Bao S; Hefti F; Thompson RF; Knusel B. 1998. Cerebellar brain-derived neurotrophic factor-TrkB defect associated with impairment of eyeblink conditioning in Stargazer mutant mice. J Neurosci 18(17):6990-9. [PubMed: 9712667] [MGI Ref ID J:49719]
Qiao X; Hefti F; Knusel B; Noebels JL. 1996. Selective failure of brain-derived neurotrophic factor mRNA expression in the cerebellum of stargazer, a mutant mouse with ataxia. J Neurosci 16(2):640-8. [PubMed: 8551348] [MGI Ref ID J:30652]
Qiao X; Noebels JL. 1993. Developmental analysis of hippocampal mossy fiber outgrowth in a mutant mouse with inherited spike-wave seizures. J Neurosci 13(11):4622-35. [PubMed: 8229188] [MGI Ref ID J:15527]
Richardson CA; Leitch B. 2002. Cerebellar Golgi, Purkinje, and basket cells have reduced gamma-aminobutyric acid immunoreactivity in stargazer mutant mice. J Comp Neurol 453(1):85-99. [PubMed: 12357434] [MGI Ref ID J:79428]
Richardson CA; Leitch B. 2005. Phenotype of cerebellar glutamatergic neurons is altered in stargazer mutant mice lacking brain-derived neurotrophic factor mRNA expression. J Comp Neurol 481(2):145-59. [PubMed: 15562504] [MGI Ref ID J:94530]
Ryu MJ; Lee C; Kim J; Shin HS; Yu MH. 2008. Proteomic analysis of stargazer mutant mouse neuronal proteins involved in absence seizure. J Neurochem 104(5):1260-70. [PubMed: 17973978] [MGI Ref ID J:131784]
Sharp AH; Black JL rd; Dubel SJ; Sundarraj S; Shen JP; Yunker AM; Copeland TD; McEnery MW. 2001. Biochemical and anatomical evidence for specialized voltage-dependent calcium channel gamma isoform expression in the epileptic and ataxic mouse, stargazer. Neuroscience 105(3):599-617. [PubMed: 11516827] [MGI Ref ID J:126681]
Song I; Kim D; Choi S; Sun M; Kim Y; Shin HS. 2004. Role of the alpha1G T-type calcium channel in spontaneous absence seizures in mutant mice. J Neurosci 24(22):5249-57. [PubMed: 15175395] [MGI Ref ID J:96913]
Thompson CL; Tehrani MHJ; Barnes EM Jr; Stephenson FA. 1998. Decreased expression of GABAA receptor alpha6 and beta3 subunits in stargazer mutant mice: a possible role for brain-derived neurotrophic factor in the regulation of cerebellar GABAA receptor expression? Brain Res Mol Brain Res 60(2):282-90. [PubMed: 9757064] [MGI Ref ID J:50701]
Zhang Y; Mori M; Burgess DL; Noebels JL. 2002. Mutations in high-voltage-activated calcium channel genes stimulate low-voltage-activated currents in mouse thalamic relay neurons. J Neurosci 22(15):6362-71. [PubMed: 12151514] [MGI Ref ID J:106959]
Zhang Y; Vilaythong AP; Yoshor D; Noebels JL. 2004. Elevated thalamic low-voltage-activated currents precede the onset of absence epilepsy in the SNAP25-deficient mouse mutant coloboma. J Neurosci 24(22):5239-48. [PubMed: 15175394] [MGI Ref ID J:96914]
Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Room Number FGB29
Colony Maintenance
Mating System Outcross-Intercross (Female x Male) 01-MAR-06 TJL Breeding Summary: homozygote x B6C3Fe a/a F1 then heterozygote x heterozygote
Purchasing information
Pricing, Supply Level & Notes, Controls, General Terms & Conditions
Pricing
| Pricing for USA, Canada and Mexico shipping destinations |
|
Weeks of Age Price (US dollars $) Gender Genotypes Provided Individual Mouse $207.10 Female or Male Homozygous for Cacng2stg
Pairs /Price (US dollars $) Pair Genotype $279.20 Heterozygous for Cacng2stg x Heterozygous for Cacng2stg
Additional Supply Details
| Pricing for International shipping destinations |
|
Weeks of Age Price (US dollars $) Gender Genotypes Provided Individual Mouse $269.30 Female or Male Homozygous for Cacng2stg
Pairs /Price (US dollars $) Pair Genotype $363.00 Heterozygous for Cacng2stg x Heterozygous for Cacng2stg
Additional Supply Details
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Supply Details
| Standard Supply | Repository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of approximately nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within two business days following order placement. |
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| Supply Notes |
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Control Information
| Control | ||
|---|---|---|
| Untyped from the colony | ||
| Considerations for Choosing Controls | ||
| USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| International - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
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JAX® Mice, Products & Services Conditions of Use
"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.No Warranty
MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.
In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.
No Liability
In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. In purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.
MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.
The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.
Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.