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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Sncgtm1Vlb
targeted mutation 1, Vladimir L Buchman
MGI:2683142
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Sncgtm1Vlb/Sncgtm1Vlb B6.129P2-Sncgtm1Vlb MGI:2683143
cx2
Sncatm1Rosl/Sncatm1Rosl
Sncgtm1Vlb/Sncgtm1Vlb
B6.129-Sncatm1Rosl Sncgtm1Vlb MGI:4417820


Genotype
MGI:2683143
hm1
Allelic
Composition
Sncgtm1Vlb/Sncgtm1Vlb
Genetic
Background
B6.129P2-Sncgtm1Vlb
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sncgtm1Vlb mutation (1 available); any Sncg mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• homozygotes are viable, fertile and display no morphological or functional abnormalities of the nervous system relative to wild-type controls (J:86439)
• normal numbers of motoneurons in five brain stem motor nuclei, including facial, oculomotor, hypoglossal, trigeminal motor, and trochlear nuclei (J:86439)
• normal numbers of sensory neurons in trigeminal ganglia and L6 lumbar dorsal root ganglia (J:86439)
• normal morphology and numbers of myelinated A-fibers and unmyelinated C-fibers in adult saphenous nerves (J:86439)
• normal survival characteristics of P2 trigenimal ganglion neurons in various culture conditions (J:86439)
• normal sensory recovery after chronic constriction injury (CCI) to the sciatic nerve, suggesting that nerve regeneration and plasticity of early somatosensory pathways remains intact (J:86439)
• no significant differences in dopamine or its metabolite (DOPAC, 5-HIAA and HVA) levels in the striatum at 9 months of age (J:92213)
• homozygotes display resistance of SNpc dopaminergic neurons to MPTP neurotoxicity
• early postnatal (P5) and adult (18 months) homozygotes show a similar (15-20%) 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
• however, no differences in the number of midbrain dopaminergic neurons are detected in SNpc at E18
• also, no significant decrease in the number of TH-positive dopaminergic neurons is noted in SNpc after methyl-phenyl-tetrahydropyridine (MPTP) treatment relative to controls

homeostasis/metabolism
• homozygotes display resistance of SNpc dopaminergic neurons to MPTP neurotoxicity

behavior/neurological
N
• adult male homozygotes show normal behavioral reflex responses to noxious radiant heat and graded mechanical stimuli in the CCI model of neuropathic pain (J:86439)
• homozygotes are behaviorally normal and show no detectable motor dysfunction in either constant speed or accelerating rotarod tests (J:92213)

cellular
• homozygotes display resistance of SNpc dopaminergic neurons to MPTP neurotoxicity




Genotype
MGI:4417820
cx2
Allelic
Composition
Sncatm1Rosl/Sncatm1Rosl
Sncgtm1Vlb/Sncgtm1Vlb
Genetic
Background
B6.129-Sncatm1Rosl Sncgtm1Vlb
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sncatm1Rosl mutation (4 available); any Snca mutation (36 available)
Sncgtm1Vlb mutation (1 available); any Sncg mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• double homozygotes are viable, fertile and display no gross abnormalities of the nervous system
• no significant differences in dopamine or its metabolite (DOPAC, 5-HIAA and HVA) levels are noted in the striatum at 9 months of age
• similar to single homozygotes, double homozygotes display resistance of SNpc dopaminergic neurons to MPTP neurotoxicity
• adult double 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 single homozygotes
• 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

homeostasis/metabolism
• similar to single homozygotes, double homozygotes display resistance of SNpc dopaminergic neurons to MPTP neurotoxicity

behavior/neurological
N
• double homozygotes are behaviorally normal and show no detectable motor dysfunction in either constant speed or accelerating rotarod tests

cellular
• similar to single homozygotes, double homozygotes display resistance of SNpc dopaminergic neurons to MPTP neurotoxicity





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last database update
10/29/2024
MGI 6.24
The Jackson Laboratory