Search Criteria: Research Area is "Neurobiology Research: Parkinson's Disease (synuclein mutants)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 008473 | B6.Cg-Tg(THY1-SNCA*A30P)M30Sud/J | Repository- Live |
| The A30P mutation in this transgenic strain is associated with the development of familial Parkinson's disease. The onset of hind limb mobility problems and a resting tremor phenotype occur around 10 months of age due to a loss of motor neurons. No Lewy body-like pathology has been observed. Extensive cell death in the spinal cord and brain are seen. This strain may be useful in studies of Parkinson's disease. Expression of the transgene is 5-fold higher in the brain and 10-fold higher in the spinal cord. Hemizygous mice are viable and fertile, and survive to approximately 14 months of age. | ||
| 008135 | B6.Cg-Tg(THY1-SNCA*A53T)M53Sud/J | Repository- Live |
| Hemizygous transgenic mice are viable and fertile and develop a Parkinson-like phenotype upon aging. Hind limb paralysis due to loss of motor neurons and a resting tremor are initially seen at about six months of age. No Lewy body-like pathology is noted. Cell death in the spinal cord (extensive) and brain are observed. | ||
| 006390 | B6;129-Sncatm1Sud Sncbtm1.1Sud/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. No protein product from these targeted genes is detected in brain tissue. Overall brain morphology and structure appears normal. No significant changes in the ultrastructure, short- or long-term synaptic plasticity, or in the pool size or replenishment of recycling synaptic vesicles is detected. Dopamine levels in the double targeted mice are decreased by approximately 20%, but dopamine uptake and release from isolated nerve terminals is normal. Serotonin levels are unchanged. This mutant mouse strain represents a model that may be useful in studies of synaptic function and neurodegenerative disease. | ||
| 003692 | B6;129X1-Sncatm1Rosl/J | Repository- Live |
| 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. | ||
| 004479 | B6;C3-Tg(Prnp-SNCA*A53T)83Vle/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable and normal in size. These transgenic mice express human A53T variant alpha-synuclein (full-length, 140 amino acid isoform) under the direction of the mouse prion protein promoter. At eight months of age, some homozygous mice develop a progressively severe motor phenotype. Presentation of the phenotype may manifest at 14-15 months of age (on average). Lax grooming, weight loss and diminished mobility precede movement impairment, partial limb paralysis, trembling and inability to stand. Immunohistochemistry analysis of mutants between eight to 12 months of age reveals widely distributed alpha-synuclein inclusions, with dense accumulation in the spinal cord, brainstem, cerebellum and thalamus. The appearance of alpha-synuclein aggregate inclusions parallels the onset of the motor impairment phenotype. Axons and myelin sheaths exhibit progressive ultrastructural degeneration. Immunoelectron microscopy and biochemical analysis show the in
..... For more information please see the full descriiption on the strain data sheet | ||
| 008132 | STOCK Tg(THY1-Snca)M1mSud/J | Repository- Live |
| Mice hemizygous for this transgene are viable and fertile and do not display any gross physical or behavioral abnormalities, even upon aging. This strain may be useful in studies of presynaptic proteins and synaptic vesicles. | ||
| 008133 | B6.129-Sncbtm1Sud/J | Repository-Cryopreserved |
| These mice possess loxP sites on either side of exon 2 of the targeted gene. Mice that are homozygous for this allele are viable, normal in size and do not display any gross physical or behavioral abnormalities, but breed very poorly. Protein levels are normal. When bred to a strain expressing Cre recombinase, this mutant mouse strain may be useful in studies of presynaptic proteins and synaptic vesicles. | ||
| 008389 | C57BL/6-Tg(THY1-SNCA)1Sud/J | Repository-Cryopreserved |
| This transgenic strain carries a human THY1 promoter driving expression of the human synuclein, alpha (SNCA) gene. Levels of expression show a 5-fold increase in the brain and a 10-fold increase in the spinal cord. Hemizygotes are viable and fertile and unlike some similar mutant transgenic lines, do not display any Parkinson-like phenotype upon aging. | ||
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