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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Slc6a3tm1Hhg
targeted mutation 1, Howard H Gu
MGI:3653596
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Slc6a3tm1Hhg/Slc6a3tm1Hhg B6.129X1-Slc6a3tm1Hhg MGI:5318772
hm2
Slc6a3tm1Hhg/Slc6a3tm1Hhg involves: 129X1/SvJ * C57BL/6J MGI:3653646


Genotype
MGI:5318772
hm1
Allelic
Composition
Slc6a3tm1Hhg/Slc6a3tm1Hhg
Genetic
Background
B6.129X1-Slc6a3tm1Hhg
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc6a3tm1Hhg mutation (1 available); any Slc6a3 mutation (32 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• in an open-field test, mutants display higher horizontal activity than controls

nervous system
• sensitivity of cannabinoid CB1 receptors (CB1Rs) controlling GABA-mediated synaptic currents in the striatum is lost, however CB1Rs modulating glutamate transmission and GABAB receptors are not affected
• the effects of CB1R agonist HU210 on striatal neuron spontaneous inhibitory postsynaptic currents (sIPSCs) and evoked inhibitory postsynaptic currents (eIPSCs) are abolished, indicating loss of sensitivity of CB1Rs(GABA)
• however, the GABAB receptor agonist baclofen has the same effect as in controls
• cocaine or sucrose are unable to alter the HU210 effects on sIPSCs as they do in control mice
• dihydroxyphenylglycine treatment does not inhibit striatal miniature inhibitory postsynaptic current (mIPSC) frequency as in wild-type mice

Mouse Models of Human Disease
OMIM ID Ref(s)
Attention Deficit-Hyperactivity Disorder; ADHD 143465 J:183177




Genotype
MGI:3653646
hm2
Allelic
Composition
Slc6a3tm1Hhg/Slc6a3tm1Hhg
Genetic
Background
involves: 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc6a3tm1Hhg mutation (1 available); any Slc6a3 mutation (32 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mutants given four injections of 5 and 20 mg/kg cocaine fail to develop a conditioned placement preference compared to robust CPP in wild-type at these doses
• 2.5 mg/kg of amphetamine induces similar levels of CPP in mutants and wild-type
• doses of cocaine from 10-40 mg/kg had no effect on mutants but increased activity significantly in wild-type mice; cocaine induced locomotor suppression in a dose-dependent fashion in mutants
• 10 mg/kg morphine or amphetamine stimulated locomotor activity in mutants but not in wild-type
• mutants display higher baseline motor activity than wild-type

nervous system
• spontaneous firing by wild-type dopaminergic neurons in brain slices is inhibited by 53.2% by a dose of 5 um cocaine but there is no significant effect on mutant neurons
• extracellular dopamine concentrations in freely-moving mice measured by microdialysis are 64% higher than in wild-type mice
• amplitude of dopamine release is 25% lower and decay is 3-fold slower in mutants compared to wild-type as assessed by fast cyclic voltammetry
• release of dopamine in response to amphetamine is lower than in wild-type
• ins synaptosomal uptake assays, the mutant dopamine transporters are 89-fold more sensitive to cocaine inhibition than those from wild-type mice





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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
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last database update
05/17/2016
MGI 6.03
The Jackson Laboratory