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- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
- Terms of Use
Description
The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.
Strain Information
Type Congenic; Mutant Strain; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Background Strain C57BL/6J Donor Strain DBA/2J Generation N26p
Generation DefinitionsAppearance
black, ataxic
Related Genotype: a/a Cacna1atg/Cacna1atg
black, unaffected
Related Genotype: a/a +/? or a/a Cacna1atg/+Description
Mice homozygous for the tottering spontaneous mutation (Cacna1atg) are characterized by a wobbly gait beginning at around 3 to 4 weeks of age and affecting, particularly, the hindquarters and by intermittent, spontaneous seizures. The seizures are of two kinds: i) Sudden arrests of movement (behavioral absence seizures) begin at about 3 weeks and are accompanied by abnormal bursts of bilaterally synchronous spike waves in ECG; they last about 0.3 to 10 seconds, occur hundreds of times per day, and continue throughout life; ii) Stereotyped partial motor seizures begin at about 4 weeks and are accompanied by abnormal ECG activity; they last 20 to 30 minutes, occur once or twice a day, and persist throughout life. Homozygous mutant mice of both sexes are fertile, but breeding performance is poor.Leaner/tottering heterozygotes (Cacna1atg-la/Cacna1atg) show ataxia, stiffness, and retarded motor activity at 15 to 17 days of age. Within a few days, they develop a wobbly gait and intermittent focal seizures which continue throughout life.
Control Information
| Control | ||
|---|---|---|
| Untyped from the colony | ||
| Considerations for Choosing Controls | ||
Related Strains
Parkinson's Disease Models
View Parkinson's Disease Models (99 strains)
008623 B10.Cg-Cacna1aTg-5J/LetJ 008816 B6.129S7-Cacna1atm1Hzo/J 008815 B6.129S7-Cacna1atm2Hzo/J 008683 B6.129S7-Cacna1atm3Hzo/J 008622 B6.C3Bir-Cacna1atg-4J/LetJ 000566 B6.Cg-Os +/+ Cacna1atg-la/J 005520 B6;CByJ-Cacna1atg-6J/J
Additional Web Information
Visit the Parkinson's Disease Resource site for helpful information on Parkinson's and research resources.
Phenotype
Phenotype Information
assigned by genotype
Cacna1atg/Cacna1atg
B6.D2-Cacna1atg/J
- nervous system phenotype
- abnormal paired-pulse inhibition
- PPI is observed at 50 msecond interpulse interval, but is reduced compared to wild-type or Cacna1tg-rol homozygotes in young, non-ataxic mutants; PPI is further reduced in adult ataxic mice compared to young mutants (MGI Ref ID J:109231)
- decreased excitatory postsynaptic current amplitude
- parallel fiber (PF) stimulation is less effective in eliciting EPSCs in ataxic mutants than in wild-type at stimulation intensities of 3-15 Volts (MGI Ref ID J:109231)
- EPSCs in mice aged 14-20 days (non-ataxic) show a 30% reduction in amplitude; mice aged 28-35 days (ataxic) show a 70% reduction in EPSC amplitude (MGI Ref ID J:109231)
- when the P/Q-type calcium channel blocker agatoxin is applied to brain slices, PF-EPSCs are reduced in amplitude by 60% compared to wild-type (MGI Ref ID J:109231)
- behavior/neurological phenotype
- ataxia
- mice show ataxic behavior around 3-4 weeks of age (MGI Ref ID J:109231)
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Cacna1atg/Cacna1atg
involves: C57BL/6J * DBA/2J
- nervous system phenotype
- abnormal CNS synaptic transmission
- peak current densities of low voltage-activated (LVA) calcium channels in thalamocortical (TC) neurons at membrane potential of -50 mV are increased by 46% compared to control (MGI Ref ID J:106959)
- peak current densities of high voltage calcium channels (HVA) in TC neurons are increased compared to wild-type (MGI Ref ID J:106959)
This mouse can be used to support research in many areas including:
Cacna1atg relatedNeurobiology Research
Parkinson's Disease
resistance to MPTP
Cell Biology Research
Channel and Transporter Defects
calcium
Mouse/Human Gene Homologs
migraine, familial hemiplegic, with progressive cerebellar ataxia
Neurobiology Research
Ataxia (Movement) Defects
Cerebellar Defects
Channel and Transporter Defects
calcium
Epilepsy
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Cacna1atg | ||
|---|---|---|---|
| Allele Name | tottering | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | alpha1Atg; tg; | ||
| Strain of Origin | DBA/2J | ||
| Gene Symbol and Name | Cacna1a, calcium channel, voltage-dependent, P/Q type, alpha 1A subunit | ||
| Chromosome | 8 | ||
| Gene Common Name(s) | APCA; BI; BccA1; CACNL1A4; CAV2.1; Ccha1a; EA2; FHM; HPCA; MHP; MHP1; SCA6; alpha1A; calcium channel alpha 1a; la; leaner; neuroscience mutagenesis facility, 352; nmf352; rbA-1; rkr; rocker; tg; tottering; | ||
| General Note | Cacna1atg, tottering, recessive. The tg mutation arose spontaneously in the DBA/2 inbred strain. Cacna1atg homozygotes are characterized by a wobbly gait affecting the hindquarters in particular, which begins at about 3 to 4 weeks of age, and by intermittent spontaneous seizures. The seizures are of two kinds, sudden arrrest of movement and stereotyped partial motor seizures (J:262).Sudden arrests of movement (behavioral absence seizures) begin at about 3 weeks of age and are accompanied by abnormal bursts of bilaterally synchronous spike waves in electrocorticograms (EEG); they last about 0.3 to 10.0 seconds, occur hundreds of times per day, and continue throughout life (J:6154). Resemblance to human epileptic absence seizures suggests the use of these mutants in epilepsy research (J:1254). Prolonged paroxysmal depolarizing shifts in hippocampal pyramidal neurons of tottering mice occur in response to elevated extracellular potassium and are age-correlated with the appearance of seizures (J:1180). Genetically altered sensitivity to increased K+, however, is not the cause of the hyperexcitability of hippocampal neurons in mutant mice (J:15775).Stereotyped partial motor seizures begin at about 4 weeks of age and are accompanied by abnormal EEG activity; they last 20 to 30 minutes, occur once or twice a day, and persist throughout life (J:6154). The central nervous system appears normal by light microscopy (J:7519). There is no discernible cerebellar hypoplasia (J:15016).In fluorescent histochemistry studies Cacna1atg homozygous mice show a marked increase in number of noradrenergic fibers in the terminal fields innervated by locus ceruleus axons, the hippocampus, cerebellum, and dorsal lateral geniculate (J:6615). Treatment of neonatal mutant mice with 6-hydroxydopamine, which selectively causes degeneration of distal noradrenergic axons from the locus ceruleus, almost completely abolishes the ataxic and seizure symptoms and the abnormal EEG patterns (J:7519). These results suggest that the primary effect of Cacna1atg may be in the neurons of the locus ceruleus. However, there was no quantitative difference in tyrosine hydroxylase (TH) mRNA or protein in the locus ceruleus of Cacna1atg/Cacna1atg or Cacna1atg/Cacna1atg-la mice, whereas these mutants expressed high levels of TH mRNA and protein in cerebellar Purkinje cells (J:2495). Normal cerebellar Purkinje cells express TH transiently during development, but expression persists into adulthood in mutant mice (J:10927). Levels of oxidized glutathione are lowered in hippocampus and occipital cortex of Cacna1atg homozygotes, whereas reduced glutathione was lowered in the cerebellum (J:28460). The level of methionine-enkephalin, but not those of ß-endorphin or dynorphin, was increased in several brain areas (J:633).Viability of Cacna1atg homozygotes is nearly normal. Homozygotes of both sexes are fertile, but breeding performance is low (J:262). | ||
| Molecular Note | The C to T transition point mutation is predicted to result in a replacement of leucine for proline in a conserved domain of the protein. [MGI Ref ID J:38910] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Cacna1atg, Separated PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
Fletcher CF; Lutz CM; O'Sullivan TN; Shaughnessy JD Jr; Hawkes R; Frankel WN; Copeland NG; Jenkins NA. 1996. Absence epilepsy in tottering mutant mice is associated with calcium channel defects. Cell 87(4):607-17. [PubMed: 8929530] [MGI Ref ID J:36596]
Meier H; MacPike AD. 1971. Three syndromes produced by two mutant genes in the mouse. Clinical, pathological, and ultrastructural bases of tottering, leaner, and heterozygous mice. J Hered 62(5):297-302. [PubMed: 4941467] [MGI Ref ID J:5240]
Noebels JL; Sidman RL. 1979. Inherited epilepsy: spike-wave and focal motor seizures in the mutant mouse tottering. Science 204(4399):1334-6. [PubMed: 572084] [MGI Ref ID J:6154]
Additional References
Abbott LC; Nejad HH; Bottje WG; Hassan AS. 1990. Glutathione levels in specific brain regions of genetically epileptic (tg/tg) mice. Brain Res Bull 25(4):629-31. [PubMed: 2271967] [MGI Ref ID J:28460]
Kostopoulos GK. 1992. The tottering mouse: a critical review of its usefulness in the study of the neuronal mechanisms underlying epilepsy. J Neural Transm Suppl 35:21-36. [PubMed: 1512593] [MGI Ref ID J:1254]
Cacna1atg relatedAbbott LC; Nejad HH; Bottje WG; Hassan AS. 1990. Glutathione levels in specific brain regions of genetically epileptic (tg/tg) mice. Brain Res Bull 25(4):629-31. [PubMed: 2271967] [MGI Ref ID J:28460]
Austin MC; Schultzberg M; Abbott LC; Montpied P; Evers JR; Paul SM; Crawley JN. 1992. Expression of tyrosine hydroxylase in cerebellar Purkinje neurons of the mutant tottering and leaner mouse. Brain Res Mol Brain Res 15(3-4):227-40. [PubMed: 1279353] [MGI Ref ID J:2495]
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]
Baurle J; Hoshi M; Grusser-Cornehls U. 1998. Dependence of parvalbumin expression on Purkinje cell input in the deep cerebellar nuclei. J Comp Neurol 392(4):499-514. [PubMed: 9514513] [MGI Ref ID J:118391]
Caddick SJ; Wang C; Fletcher CF; Jenkins NA; Copeland NG; Hosford DA. 1999. Excitatory but not inhibitory synaptic transmission is reduced in lethargic (Cacnb4(lh)) and tottering (Cacna1atg) mouse thalami. J Neurophysiol 81(5):2066-74. [PubMed: 10322048] [MGI Ref ID J:56225]
Campbell DB; Hess EJ. 1998. Cerebellar circuitry is activated during convulsive episodes in the tottering (tg/tg) mutant mouse. Neuroscience 85(3):773-83. [PubMed: 9639271] [MGI Ref ID J:48108]
Campbell DB; Hess EJ. 1996. Chromosomal localization of the neurological mouse mutations tottering (tg), Purkinje cell degeneration (pcd), and nervous (nr). Brain Res Mol Brain Res 37(1-2):79-84. [PubMed: 8738138] [MGI Ref ID J:33012]
Campbell DB; Hess EJ. 1999. L-type calcium channels contribute to the tottering mouse dystonic episodes. Mol Pharmacol 55(1):23-31. [PubMed: 9882694] [MGI Ref ID J:52508]
Campbell DB; North JB; Hess EJ. 1999. Tottering mouse motor dysfunction is abolished on the Purkinje cell degeneration (pcd) mutant background. Exp Neurol 160(1):268-78. [PubMed: 10630211] [MGI Ref ID J:58539]
Cicale M; Ambesi-Impiombato A; Cimini V; Fiore G; Muscettola G; Abbott LC; de Bartolomeis A. 2002. Decreased gene expression of calretinin and ryanodine receptor type 1 in tottering mice. Brain Res Bull 59(1):53-8. [PubMed: 12372549] [MGI Ref ID J:102589]
Colliver TL; Hess EJ; Ewing AG. 2001. Amperometric analysis of exocytosis at chromaffin cells from genetically distinct mice. J Neurosci Methods 105(1):95-103. [PubMed: 11166370] [MGI Ref ID J:102977]
Cope DW; Di Giovanni G; Fyson SJ; Orban G; Errington AC; Lorincz ML; Gould TM; Carter DA; Crunelli V. 2009. Enhanced tonic GABAA inhibition in typical absence epilepsy. Nat Med 15(12):1392-8. [PubMed: 19966779] [MGI Ref ID J:155872]
De Bartolomeis A; Koprivica V; Pickar D; Crawley JN; Abbott LC. 1997. Opioidergic and dopaminergic gene expression in the caudate-putamen and accumbens of the mutant mouse, tottering (tg/tg). Brain Res Mol Brain Res 46(1-2):321-4. [PubMed: 9191109] [MGI Ref ID J:40443]
Dove LS; Abbott LC; Griffith WH. 1998. Whole-cell and single-channel analysis of P-type calcium currents in cerebellar Purkinje cells of leaner mutant mice. J Neurosci 18(19):7687-99. [PubMed: 9742139] [MGI Ref ID J:112100]
Doyle J; Ren X; Lennon G; Stubbs L. 1997. Mutations in the Cacnl1a4 calcium channel gene are associated with seizures, cerebellar degeneration, and ataxia in tottering and leaner mutant mice. Mamm Genome 8(2):113-20. [PubMed: 9060410] [MGI Ref ID J:38910]
Erickson MA; Haburcak M; Smukler L; Dunlap K. 2007. Altered functional expression of Purkinje cell calcium channels precedes motor dysfunction in tottering mice. Neuroscience 150(3):547-55. [PubMed: 18023294] [MGI Ref ID J:130760]
Etheredge JA; Murchison D; Abbott LC; Griffith WH. 2007. Functional compensation by other voltage-gated Ca2+ channels in mouse basal forebrain neurons with Ca(V)2.1 mutations. Brain Res 1140:105-19. [PubMed: 16364258] [MGI Ref ID J:120185]
Frank-Cannon TC; Zeve DR; Abbott LC. 2007. Developmental expression of neuronal nitric oxide synthase in P/Q-type voltage-gated calcium ion channel mutant mice, leaner and tottering. Brain Res 1140:96-104. [PubMed: 16359645] [MGI Ref ID J:120186]
Fureman BE; Hess EJ. 2005. Noradrenergic blockade prevents attacks in a model of episodic dysfunction caused by a channelopathy. Neurobiol Dis 20(2):227-32. [PubMed: 16242631] [MGI Ref ID J:102801]
GREEN MC; SIDMAN RL. 1962. Tottering--a neuromusclar mutation in the mouse. And its linkage with oligosyndacylism. J Hered 53:233-7. [PubMed: 13950100] [MGI Ref ID J:262]
Glasscock E; Qian J; Yoo JW; Noebels JL. 2007. Masking epilepsy by combining two epilepsy genes. Nat Neurosci 10(12):1554-8. [PubMed: 17982453] [MGI Ref ID J:130784]
Helekar SA; Noebels JL. 1992. A burst-dependent hippocampal excitability defect elicited by potassium at the developmental onset of spike-wave seizures in the Tottering mutant. Brain Res Dev Brain Res 65(2):205-10. [PubMed: 1572065] [MGI Ref ID J:1180]
Helekar SA; Noebels JL. 1994. Analysis of voltage-gated and synaptic conductances contributing to network excitability defects in the mutant mouse tottering. J Neurophysiol 71(1):1-10. [PubMed: 8158221] [MGI Ref ID J:18102]
Hess EJ; Wilson MC. 1991. Tottering and leaner mutations perturb transient developmental expression of tyrosine hydroxylase in embryologically distinct Purkinje cells. Neuron 6(1):123-32. [PubMed: 1670919] [MGI Ref ID J:10927]
Hoebeek FE; Stahl JS; van Alphen AM; Schonewille M; Luo C; Rutteman M; van den Maagdenberg AM; Molenaar PC; Goossens HH; Frens MA; De Zeeuw CI. 2005. Increased noise level of purkinje cell activities minimizes impact of their modulation during sensorimotor control. Neuron 45(6):953-65. [PubMed: 15797555] [MGI Ref ID J:99672]
Iasevoli F; Cicale M; Abbott LC; de Bartolomeis A. 2011. Striatal expression of Homer1a is affected by genotype but not dystonic phenotype of tottering mice: a model of spontaneously occurring motor disturbances. Neurosci Lett 503(3):176-80. [PubMed: 21884752] [MGI Ref ID J:178558]
Isaacs KR; Abbott LC. 1995. Cerebellar volume decreases in the tottering mouse are specific to the molecular layer. Brain Res Bull 36(3):309-14. [PubMed: 7697385] [MGI Ref ID J:22482]
Isaacs KR; Abbott LC. 1992. Development of the paramedian lobule of the cerebellum in wild-type and tottering mice. Dev Neurosci 14(5-6):386-93. [PubMed: 1306163] [MGI Ref ID J:14500]
Kaja S; Van de Ven RC; Ferrari MD; Frants RR; Van den Maagdenberg AM; Plomp JJ. 2006. Compensatory contribution of Cav2.3 channels to acetylcholine release at the neuromuscular junction of tottering mice. J Neurophysiol 95(4):2698-704. [PubMed: 16381801] [MGI Ref ID J:135773]
Kilbourn MR; Sherman P; Abbott LC. 1998. Reduced MPTP neurotoxicity in striatum of the mutant mouse tottering. Synapse 30(2):205-10. [PubMed: 9723790] [MGI Ref ID J:51445]
Kilbourn MR; Sherman PS; Abbott LC. 1995. Mutant mouse strains as models for in vivo radiotracer evaluations: [11C]methoxytetrabenazine ([11C]MTBZ) in tottering mice. Nucl Med Biol 22(5):565-7. [PubMed: 7581164] [MGI Ref ID J:28256]
Kostopoulos GK. 1992. The tottering mouse: a critical review of its usefulness in the study of the neuronal mechanisms underlying epilepsy. J Neural Transm Suppl 35:21-36. [PubMed: 1512593] [MGI Ref ID J:1254]
Kostopoulos GK; Psarropoulou CT. 1992. Possible mechanisms underlying hyperexcitability in the epileptic mutant mouse tottering. J Neural Transm Suppl 35:109-24. [PubMed: 1355109] [MGI Ref ID J:3627]
Koyanagi Y; Sawada K; Sakata-Haga H; Jeong YG; Fukui Y. 2006. Increased serotonergic innervation of lumbosacral motoneurons of rolling mouse Nagoya in correlation with abnormal hindlimb extension. Anat Histol Embryol 35(6):387-92. [PubMed: 17156092] [MGI Ref ID J:135940]
Krause KH; Bonjour JP; Aichele-Wehrse R; Huck-Breiter M; Berlit P. 1997. Effect of biotin depletion on spike-wave seizures in the tottering mutant mouse. Int J Vitam Nutr Res 67(6):461-3. [PubMed: 9433681] [MGI Ref ID J:45255]
Leenders AG; van den Maagdenberg AM; Lopes da Silva FH; Sheng ZH; Molenaar PC; Ghijsen WE. 2002. Neurotransmitter release from tottering mice nerve terminals with reduced expression of mutated P- and Q-type Ca2+-channels. Eur J Neurosci 15(1):13-8. [PubMed: 11860502] [MGI Ref ID J:108143]
Levitt P; Noebels JL. 1981. Mutant mouse tottering: selective increase of locus ceruleus axons in a defined single-locus mutation. Proc Natl Acad Sci U S A 78(7):4630-4. [PubMed: 6945603] [MGI Ref ID J:6615]
Matsushita K; Wakamori M; Rhyu IJ; Arii T; Oda S; Mori Y; Imoto K. 2002. Bidirectional alterations in cerebellar synaptic transmission of tottering and rolling Ca2+ channel mutant mice. J Neurosci 22(11):4388-98. [PubMed: 12040045] [MGI Ref ID J:109231]
Nakane K. 1976. Postnatal development of brain with congenital ataxia, rolling (rol) and tottering (tg). Teratology 14:248-49. [MGI Ref ID J:15016]
Noebels JL. 1984. A single gene error of noradrenergic axon growth synchronizes central neurones. Nature 310(5976):409-11. [PubMed: 6462226] [MGI Ref ID J:7519]
Oda SI. 1981. A new allele of the tottering locus, rolling mouse Nagoya, on Chromosome no. 8 in the mouse Jpn J Genet 56:295-99. [MGI Ref ID J:14882]
Patel VK; Abbott LC; Rattan AK; Tejwani GA. 1991. Increased methionine-enkephalin levels in genetically epileptic (tg/tg) mice. Brain Res Bull 27(6):849-52. [PubMed: 1686215] [MGI Ref ID J:633]
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]
Plomp JJ; Vergouwe MN; Van den Maagdenberg AM; Ferrari MD; Frants RR; Molenaar PC. 2000. Abnormal transmitter release at neuromuscular junctions of mice carrying the tottering alpha(1A) Ca(2+) channel mutation. Brain 123 Pt 3:463-71. [PubMed: 10686170] [MGI Ref ID J:102080]
Pralong E; Magistretti PJ. 1994. Noradrenaline reduces synaptic responses in normal and tottering mouse entorhinal cortex via alpha 2 receptors. Neurosci Lett 179(1-2):145-8. [PubMed: 7845610] [MGI Ref ID J:22066]
Psarropoulou C; Kostopoulos G. 1993. Comparison of the effects of increased potassium and of adenosine on hippocampal neurons from normal and genetically epileptic tg/tg mice. Epilepsia 34(1):24-32. [PubMed: 8380766] [MGI Ref ID J:15775]
Qian J; Noebels JL. 2000. Presynaptic Ca(2+) influx at a mouse central synapse with Ca(2+) channel subunit mutations. J Neurosci 20(1):163-70. [PubMed: 10627593] [MGI Ref ID J:120572]
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]
Rhyu IJ; Abbott LC; Walker DB; Sotelo C. 1999. An ultrastructural study of granule cell/Purkinje cell synapses in tottering (tg/tg), leaner (tg(la)/tg(la)) and compound heterozygous tottering/leaner (tg/tg(la)) mice. Neuroscience 90(3):717-28. [PubMed: 10218773] [MGI Ref ID J:106598]
Rhyu IJ; Nahm SS; Hwang SJ; Kim H; Suh YS; Oda SI; Frank TC; Abbott LC. 2003. Altered neuronal nitric oxide synthase expression in the cerebellum of calcium channel mutant mice. Brain Res 977(2):129-40. [PubMed: 12834873] [MGI Ref ID J:84467]
Sasaki S; Huda K; Inoue T; Miyata M; Imoto K. 2006. Impaired feedforward inhibition of the thalamocortical projection in epileptic Ca2+ channel mutant mice, tottering. J Neurosci 26(11):3056-65. [PubMed: 16540584] [MGI Ref ID J:106709]
Sawada K; Haga H; Fukui Y. 2000. Ataxic mutant mice with defects in Ca2+ channel alpha-1A subunit gene: morphological and functional abnormalities in cerebellar cortical neurons Cong Anom 40:99-107. [MGI Ref ID J:65744]
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]
Tehrani MH; Barnes EM Jr. 1995. Reduced function of gamma-aminobutyric acidA receptors in tottering mouse brain: role of cAMP-dependent protein kinase. Epilepsy Res 22(1):13-21. [PubMed: 8565963] [MGI Ref ID J:32181]
Tsuji S; Meier H. 1971. Evidence for allelism of leaner and tottering in the mouse. Genet Res 17(1):83-8. [PubMed: 4933322] [MGI Ref ID J:5210]
Wakamori M; Yamazaki K; Matsunodaira H; Teramoto T; Tanaka I; Niidome T; Sawada K; Nishizawa Y; Sekiguchi N; Mori E; Mori Y; Imoto K. 1998. Single tottering mutations responsible for the neuropathic phenotype of the P-type calcium channel. J Biol Chem 273(52):34857-67. [PubMed: 9857013] [MGI Ref ID J:51647]
Weisz CJ; Raike RS; Soria-Jasso LE; Hess EJ. 2005. Potassium channel blockers inhibit the triggers of attacks in the calcium channel mouse mutant tottering. J Neurosci 25(16):4141-5. [PubMed: 15843617] [MGI Ref ID J:98735]
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
Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, RG10/RG30.
Purchasing information
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
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Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $1980.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
Supply Notes
- Cryorecovery - Standard.
We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 13 and 16 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
| Pricing for International shipping destinations |
|
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Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2574.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
Supply Notes
- Cryorecovery - Standard.
We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 13 and 16 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
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Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
General Supply Notes
- This strain is included in the Mouse Mutant Resource collection.
- Genomic DNA is available for this strain from the Mouse DNA Resource.
Control Information
| Control | ||
|---|---|---|
| Untyped from the colony | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
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Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.
See Terms of Use tab for General Terms and Conditions
The Jackson Laboratory's Genotype Promise
The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.Ordering Information
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| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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. Unless prohibited by law, 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.