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| Homozygous null mice suffer from a reduction in total striatal dopamine and exhibit an attenuated locomotor response when given amphetamine. Observed phenotype suggests that Snca is an activity-dependent negative regulator of dopamine neurotransmission. | |||||||||||||||||||
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Description
Strain Information
Type Mutant Stock; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Mating System Homozygote x Homozygote (Female x Male) 26-DEC-06 Species laboratory mouse Generation [F8p]+F13 (25-MAY-12)
Generation DefinitionsDonating Investigator Dr. Arnon Rosenthal, Rinat Neuroscience Corporation Description
Homozygous null mice are viable, fertile, normal in size and do not display any gross abnormalities. No gene product (mRNA or protein) is detected in brain tissue. A wild-type complement of dopamine neurons, fibers and synaptic terminals is present and the overall brain architecture appears to be intact. They suffer from a reduction in total striatal dopamine and exhibit an attenuated locomotor response when given amphetamine. Normal dopamine release is observed upon stimulation of the nigrostriatal terminal with a single electrical pulse. When multiple stimuli are applied however, null mice exhibit an accelerated recovery of dopamine release. A similar acceleration is seen in wildtype mice in the presence of increased extracellular calcium. The phenotype observed in homozygous Snca-null mice suggests that Snca is an activity-dependent negative regulator of dopamine neurotransmission.Development
A targeting vector containing a neomycin resistance gene driven by a phosphoglycerate 1 promoter was used to disrupt Snca exons 1-2 in RW-4 embryonic stem (ES) cells. These two exons encode amino acids 1-41. Correctly targeted ES cells were injected into C57BL/6 blastocysts and chimeric animals were obtained.
Control Information
| Control | ||
|---|---|---|
| None Available | ||
| Considerations for Choosing Controls | ||
Related Strains
Parkinson's Disease Models
View Parkinson's Disease Models (109 strains)
Additional Web Information
Visit the Parkinson's Disease Resource site for helpful information on Parkinson's and research resources.
Phenotype
Phenotype Information
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Parkinson Disease 1, Autosomal Dominant; PARK1
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Dementia, Lewy Body; DLB (SNCA)
Parkinson Disease 4, Autosomal Dominant; PARK4 (SNCA)
assigned by genotype
Sncatm1Rosl/Sncatm1Rosl
involves: 129X1/SvJ * C57BL/6
- nervous system phenotype
- abnormal dopaminergic neuron morphology
- when exposed to paired electrical stimuli, striatal brain slices (containing dopamine terminals) from homozygous mice exhibit a faster dopamine release recovery as compared to wild-type (MGI Ref ID J:60151)
- dopamine discharge and reuptake in response to a single electrical pulse or a train of pulses is comparable to wild-type (MGI Ref ID J:60151)
- decreased dopamine level
- dopamine content is reduced by 18% in the striatum, however, dopamine content in the ventral midbrain and nucleus accumbens is similar to wild-type (MGI Ref ID J:60151)
- behavior/neurological phenotype
- abnormal locomotor activation
- homeostasis/metabolism phenotype
- decreased dopamine level
- dopamine content is reduced by 18% in the striatum, however, dopamine content in the ventral midbrain and nucleus accumbens is similar to wild-type (MGI Ref ID J:60151)
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Sncatm1Rosl/Sncatm1Rosl
involves: 129X1/SvJ
- immune system phenotype
- decreased susceptibility to bacterial infection
- mice do not exhibit as much dopamine neuron loss following injection of LPS into the substantia nigra as similarly treated wild-type mice (MGI Ref ID J:138194)
Sncatm1Rosl/Sncatm1Rosl
B6.129X1-Sncatm1Rosl
- nervous system phenotype
- *normal* nervous system phenotype
- at P2, homozygotes display normal numbers of sensory neurons in trigeminal ganglia and L6 lumbar dorsal root ganglia relative to wild-type controls (MGI Ref ID J:86439)
- homozygotes exhibit normal morphology and numbers of myelinated A-fibers and unmyelinated C-fibers in adult saphenous nerves relative to wild-type controls (MGI Ref ID J:86439)
- in culture, neurons from P2 peripheral (trigeminal and superior cervical) ganglia of mutant mice display the same survival rate as wild-type neurons in the presence of nerve growth factor and, as expected, fail to survive in its absence (MGI Ref ID J:86439)
- homozygotes display no gross abnormalities of the nervous system relative to wild-type controls (MGI Ref ID J:92213)
- no significant differences in dopamine or its metabolite (DOPAC, 5-HIAA and HVA) levels are noted in the striatum at 9 months of age (MGI Ref ID J:92213)
- decreased dopaminergic neuron number
- adult homozygotes show a ~20% reduction in the number of tyrosine hydroxylase (TH)-positive dopaminergic neurons in substantia nigra pars compacta (SNpc) but not in ventral tegmental area (VTA) relative to wild-type controls, similar to that observed in adult Sncgtm1Vlb homozygotes (MGI Ref ID J:92213)
- however, no significant decrease in the number of TH-positive dopaminergic neurons is observed in SNpc after methyl-phenyl-tetrahydropyridine (MPTP) treatment relative to controls (MGI Ref ID J:92213)
- decreased susceptibility to dopaminergic neuron neurotoxicity
- homozygotes display resistance of SNpc dopaminergic neurons to MPTP neurotoxicity (MGI Ref ID J:92213)
- homeostasis/metabolism phenotype
- decreased susceptibility to dopaminergic neuron neurotoxicity
- homozygotes display resistance of SNpc dopaminergic neurons to MPTP neurotoxicity (MGI Ref ID J:92213)
- behavior/neurological phenotype
- *normal* behavior/neurological phenotype
- homozygotes are behaviorally normal and show no detectable motor dysfunction in either constant speed or accelerating rotarod tests (MGI Ref ID J:92213)
- cellular phenotype
- decreased susceptibility to dopaminergic neuron neurotoxicity
- homozygotes display resistance of SNpc dopaminergic neurons to MPTP neurotoxicity (MGI Ref ID J:92213)
This mouse can be used to support research in many areas including:
Sncatm1Rosl relatedNeurobiology Research
Parkinson's Disease
resistance to MPTP
synuclein mutants
Neurobiology Research
Astrocyte Defects
Behavioral and Learning Defects
Neurodegeneration
Neurotransmitter Receptor and Synaptic Vesicle Defects
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Sncatm1Rosl | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Arnon Rosenthal | ||
| Allele Type | Targeted (knock-out) | ||
| Common Name(s) | alpha-Syn-; alpha-Synko; | ||
| Strain of Origin | 129X1/SvJ | ||
| ES Cell Line Name | RW-4 | ||
| ES Cell Line Strain | 129X1/SvJ | ||
| Gene Symbol and Name | Snca, synuclein, alpha | ||
| Chromosome | 6 | ||
| Gene Common Name(s) | NACP; PARK1; PARK4; PD1; alpha-synuclein; alphaSYN; | ||
| Molecular Note | A PGK-neo cassette was used to delete exons 1 and 2, encoding amino acids 1 through 41 as well as a 5' untranslated region. RT-PCR analysis of extracts from the brains of homozygous mutant mice, using probes for both the deleted 5' region as well the untargeted 3' region, showed an absence of transcript. Western blot analysis, immunohistochemical analysis, and in situ hybridization confirmed a lack of encoded protein in homozygous mutant mice. [MGI Ref ID J:60151] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Sncatm1Rosl,SEPARATED MELT
Sncatm1Rosl, Separated PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
Abeliovich A; Schmitz Y; Farinas I; Choi-Lundberg D; Ho WH; Castillo PE; Shinsky N; Verdugo JM; Armanini M; Ryan A; Hynes M; Phillips H; Sulzer D; Rosenthal A. 2000. Mice lacking alpha-synuclein display functional deficits in the nigrostriatal dopamine system. Neuron 25(1):239-52. [PubMed: 10707987] [MGI Ref ID J:60151]
Additional References
Sncatm1Rosl relatedAkil O; Weber CM; Park SN; Ninkina N; Buchman V; Lustig LR. 2008. Localization of synucleins in the Mammalian cochlea. J Assoc Res Otolaryngol 9(4):452-63. [PubMed: 18665422] [MGI Ref ID J:141972]
Al-Wandi A; Ninkina N; Millership S; Williamson SJ; Jones PA; Buchman VL. 2010. Absence of alpha-synuclein affects dopamine metabolism and synaptic markers in the striatum of aging mice. Neurobiol Aging 31(5):796-804. [PubMed: 19097673] [MGI Ref ID J:159589]
Alvarez-Fischer D; Henze C; Strenzke C; Westrich J; Ferger B; Hoglinger GU; Oertel WH; Hartmann A. 2008. Characterization of the striatal 6-OHDA model of Parkinson's disease in wild type and alpha-synuclein-deleted mice. Exp Neurol 210(1):182-93. [PubMed: 18053987] [MGI Ref ID J:134020]
Anwar S; Peters O; Millership S; Ninkina N; Doig N; Connor-Robson N; Threlfell S; Kooner G; Deacon RM; Bannerman DM; Bolam JP; Chandra SS; Cragg SJ; Wade-Martins R; Buchman VL. 2011. Functional alterations to the nigrostriatal system in mice lacking all three members of the synuclein family. J Neurosci 31(20):7264-74. [PubMed: 21593311] [MGI Ref ID J:173360]
Cano-Jaimez M; Perez-Sanchez F; Milan M; Buendia P; Ambrosio S; Farinas I. 2010. Vulnerability of peripheral catecholaminergic neurons to MPTP is not regulated by alpha-synuclein. Neurobiol Dis 38(1):92-103. [PubMed: 20079841] [MGI Ref ID J:159933]
Chadchankar H; Ihalainen J; Tanila H; Yavich L. 2011. Decreased reuptake of dopamine in the dorsal striatum in the absence of alpha-synuclein. Brain Res 1382:37-44. [PubMed: 21276428] [MGI Ref ID J:170114]
Chadchankar H; Yavich L. 2011. Sub-regional differences and mechanisms of the short-term plasticity of dopamine overflow in striatum in mice lacking alpha-synuclein. Brain Res 1423:67-76. [PubMed: 22000591] [MGI Ref ID J:179023]
Duka T; Rusnak M; Drolet RE; Duka V; Wersinger C; Goudreau JL; Sidhu A. 2006. Alpha-synuclein induces hyperphosphorylation of Tau in the MPTP model of parkinsonism. FASEB J 20(13):2302-12. [PubMed: 17077307] [MGI Ref ID J:129746]
Ebadi M; Sharma S. 2006. Metallothioneins 1 and 2 attenuate peroxynitrite-induced oxidative stress in Parkinson disease. Exp Biol Med (Maywood) 231(9):1576-83. [PubMed: 17018883] [MGI Ref ID J:129277]
Gao HM; Kotzbauer PT; Uryu K; Leight S; Trojanowski JQ; Lee VM. 2008. Neuroinflammation and oxidation/nitration of alpha-synuclein linked to dopaminergic neurodegeneration. J Neurosci 28(30):7687-98. [PubMed: 18650345] [MGI Ref ID J:138194]
Geng X; Lou H; Wang J; Li L; Swanson AL; Sun M; Beers-Stolz D; Watkins S; Perez RG; Drain P. 2011. alpha-Synuclein binds the K(ATP) channel at insulin-secretory granules and inhibits insulin secretion. Am J Physiol Endocrinol Metab 300(2):E276-86. [PubMed: 20858756] [MGI Ref ID J:172332]
Klivenyi P; Siwek D; Gardian G; Yang L; Starkov A; Cleren C; Ferrante RJ; Kowall NW; Abeliovich A; Beal MF. 2006. Mice lacking alpha-synuclein are resistant to mitochondrial toxins. Neurobiol Dis 21(3):541-8. [PubMed: 16298531] [MGI Ref ID J:106226]
Kokhan VS; Afanasyeva MA; Van'kin GI. 2012. alpha-Synuclein knockout mice have cognitive impairments. Behav Brain Res 231(1):226-30. [PubMed: 22469626] [MGI Ref ID J:185435]
Lou H; Montoya SE; Alerte TN; Wang J; Wu J; Peng X; Hong CS; Friedrich EE; Mader SA; Pedersen CJ; Marcus BS; McCormack AL; Di Monte DA; Daubner SC; Perez RG. 2010. Serine 129 phosphorylation reduces the ability of alpha-synuclein to regulate tyrosine hydroxylase and protein phosphatase 2A in vitro and in vivo. J Biol Chem 285(23):17648-61. [PubMed: 20356833] [MGI Ref ID J:164560]
Luk KC; Kehm V; Carroll J; Zhang B; O'Brien P; Trojanowski JQ; Lee VM. 2012. Pathological alpha-synuclein transmission initiates Parkinson-like neurodegeneration in nontransgenic mice. Science 338(6109):949-53. [PubMed: 23161999] [MGI Ref ID J:191204]
Luk KC; Kehm VM; Zhang B; O'Brien P; Trojanowski JQ; Lee VM. 2012. Intracerebral inoculation of pathological alpha-synuclein initiates a rapidly progressive neurodegenerative alpha-synucleinopathy in mice. J Exp Med 209(5):975-86. [PubMed: 22508839] [MGI Ref ID J:185142]
Martin ED; Gonzalez-Garcia C; Milan M; Farinas I; Cena V. 2004. Stressor-related impairment of synaptic transmission in hippocampal slices from alpha-synuclein knockout mice. Eur J Neurosci 20(11):3085-91. [PubMed: 15579163] [MGI Ref ID J:101275]
Martin-Clemente B; Alvarez-Castelao B; Mayo I; Sierra AB; Diaz V; Milan M; Farinas I; Gomez-Isla T; Ferrer I; Castano JG. 2004. alpha-Synuclein expression levels do not significantly affect proteasome function and expression in mice and stably transfected PC12 cell lines. J Biol Chem 279(51):52984-90. [PubMed: 15466467] [MGI Ref ID J:118517]
Mosharov EV; Larsen KE; Kanter E; Phillips KA; Wilson K; Schmitz Y; Krantz DE; Kobayashi K; Edwards RH; Sulzer D. 2009. Interplay between cytosolic dopamine, calcium, and alpha-synuclein causes selective death of substantia nigra neurons. Neuron 62(2):218-29. [PubMed: 19409267] [MGI Ref ID J:155071]
Ninkina N; Papachroni K; Robertson DC; Schmidt O; Delaney L; O'Neill F; Court F; Rosenthal A; Fleetwood-Walker SM; Davies AM; Buchman VL. 2003. Neurons expressing the highest levels of gamma-synuclein are unaffected by targeted inactivation of the gene. Mol Cell Biol 23(22):8233-45. [PubMed: 14585981] [MGI Ref ID J:86439]
Papachroni K; Ninkina N; Wanless J; Kalofoutis AT; Gnuchev NV; Buchman VL. 2005. Peripheral sensory neurons survive in the absence of alpha- and gamma-synucleins. J Mol Neurosci 25(2):157-64. [PubMed: 15784963] [MGI Ref ID J:121324]
Pelkonen A; Yavich L. 2011. Neuromuscular pathology in mice lacking alpha-synuclein. Neurosci Lett 487(3):350-3. [PubMed: 21029764] [MGI Ref ID J:168149]
Rappley I; Myers DS; Milne SB; Ivanova PT; Lavoie MJ; Brown HA; Selkoe DJ. 2009. Lipidomic profiling in mouse brain reveals differences between ages and genders, with smaller changes associated with alpha-synuclein genotype. J Neurochem 111(1):15-25. [PubMed: 19627450] [MGI Ref ID J:153557]
Reznichenko L; Cheng Q; Nizar K; Gratiy SL; Saisan PA; Rockenstein EM; Gonzalez T; Patrick C; Spencer B; Desplats P; Dale AM; Devor A; Masliah E. 2012. In vivo alterations in calcium buffering capacity in transgenic mouse model of synucleinopathy. J Neurosci 32(29):9992-8. [PubMed: 22815513] [MGI Ref ID J:186464]
Robertson DC; Schmidt O; Ninkina N; Jones PA; Sharkey J; Buchman VL. 2004. Developmental loss and resistance to MPTP toxicity of dopaminergic neurones in substantia nigra pars compacta of gamma-synuclein, alpha-synuclein and double alpha/gamma-synuclein null mutant mice. J Neurochem 89(5):1126-36. [PubMed: 15147505] [MGI Ref ID J:92213]
Scott D; Roy S. 2012. alpha-Synuclein Inhibits Intersynaptic Vesicle Mobility and Maintains Recycling-Pool Homeostasis. J Neurosci 32(30):10129-35. [PubMed: 22836248] [MGI Ref ID J:186545]
Senior SL; Ninkina N; Deacon R; Bannerman D; Buchman VL; Cragg SJ; Wade-Martins R. 2008. Increased striatal dopamine release and hyperdopaminergic-like behaviour in mice lacking both alpha-synuclein and gamma-synuclein. Eur J Neurosci 27(4):947-57. [PubMed: 18333965] [MGI Ref ID J:132938]
Sharon R; Bar-Joseph I; Mirick GE; Serhan CN; Selkoe DJ. 2003. Altered fatty acid composition of dopaminergic neurons expressing alpha-synuclein and human brains with alpha-synucleinopathies. J Biol Chem 278(50):49874-81. [PubMed: 14507911] [MGI Ref ID J:118570]
Tomas-Zapico C; Diez-Zaera M; Ferrer I; Gomez-Ramos P; Moran MA; Miras-Portugal MT; Diaz-Hernandez M; Lucas JJ. 2012. alpha-Synuclein accumulates in huntingtin inclusions but forms independent filaments and its deficiency attenuates early phenotype in a mouse model of Huntington's disease. Hum Mol Genet 21(3):495-510. [PubMed: 22045698] [MGI Ref ID J:179713]
Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Room Number AX11
Colony Maintenance
Breeding & Husbandry This strain arose on a B6;129X background. It is maintained on a B6;129X background. Coat color expected from breeding:Black or Agouti Mating System Homozygote x Homozygote (Female x Male) 26-DEC-06 Diet Information LabDiet® 5K52/5K67
Pricing and Purchasing
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
|
Live Mice
Price per mouse (US dollars $) Gender Genotypes Provided Individual Mouse $177.00 Female or Male Homozygous for Sncatm1Rosl
Price per Pair (US dollars $) Pair Genotype $354.00 Homozygous for Sncatm1Rosl x Homozygous for Sncatm1Rosl Standard Supply
Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
| Pricing for International shipping destinations |
|
Live Mice
Price per mouse (US dollars $) Gender Genotypes Provided Individual Mouse $230.10 Female or Male Homozygous for Sncatm1Rosl
Price per Pair (US dollars $) Pair Genotype $460.20 Homozygous for Sncatm1Rosl x Homozygous for Sncatm1Rosl Standard Supply
Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
|
|
|
Standard Supply
Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
General Supply Notes
- Genomic DNA is available for this strain from the Mouse DNA Resource.
Control Information
| Control | ||
|---|---|---|
| None Available | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
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