ArticlePloS one2014
Unaltered striatal dopamine release levels in young Parkin knockout, Pink1 knockout, DJ-1 knockout and LRRK2 R1441G transgenic mice.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Article
- Parkinson's disease mutant Miro1 causes mitochondrial dysfunction and dopaminergic neuron loss.Brain : a journal of neurology · 2025Article
- Critical analysis of translational potential of rodent models of white matter pathology across a wide spectrum of human diseases.Cell death & disease · 2025Review
- Compensatory synaptotagmin-11 expression conceals parkinson's disease-like phenotypes in parkin knockout mice.Cell communication and signaling : CCS · 2025Article
- Modeling Parkinson's disease in LRRK2 rodents.Neuronal signaling · 2023Review
- Impaired dopamine release in Parkinson's disease.Brain : a journal of neurology · 2023Review
- Article
- Parkinson's Disease: Exploring Different Animal Model Systems.International journal of molecular sciences · 2023Review
- Amphetamine maintenance therapy during intermittent cocaine self-administration in rats attenuates psychomotor and dopamine sensitization and reduces addiction-like behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Historical Perspective: Models of Parkinson's Disease.International journal of molecular sciences · 2020Review
- From Synaptic Dysfunction to Neuroprotective Strategies in Genetic Parkinson's Disease: Lessons From LRRK2.Frontiers in cellular neuroscience · 2020Review
- Loss of PINK1 causes age-dependent decrease of dopamine release and mitochondrial dysfunction.Neurobiology of aging · 2019Article
- Crosstalk between presynaptic trafficking and autophagy in Parkinson's disease.Neurobiology of disease · 2019Review
- Early Dyskinesias in Parkinson's Disease Patients With Parkin Mutation: A Primary Corticostriatal Synaptopathy?Frontiers in neuroscience · 2019Review
- Mutant LRRK2 mediates peripheral and central immune responses leading to neurodegeneration in vivo.Brain : a journal of neurology · 2018Article
- Characterization of Dopaminergic System in the Striatum of Young Adult Park2Scientific reports · 2018Article
- Parkinson's disease: animal models and dopaminergic cell vulnerability.Frontiers in neuroanatomy · 2014Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is one of the most prevalent neurodegenerative brain diseases; it is accompanied by extensive loss of dopamine (DA) neurons of the substantia nigra that project to the putamen, leading to impaired motor functions. Several genes have been associated with hereditary forms of the disease and transgenic mice have been developed by a number of groups to produce animal models of PD and to explore the basic functions of these genes. Surprisingly, most of the various mouse lines generated such as Parkin KO, Pink1 KO, DJ-1 KO and LRRK2 transgenic have been reported to lack degeneration of nigral DA neuron, one of the hallmarks of PD. However, modest impairments of motor behavior have been reported, suggesting the possibility that the models recapitulate at least some of the early stages of PD, including early dysfunction of DA axon terminals. To further evaluate this possibility, here we provide for the first time a systematic comparison of DA release in four different mouse lines, examined at a young age range, prior to potential age-dependent compensations. Using fast scan cyclic voltammetry in striatal sections prepared from young, 6-8 weeks old mice, we examined sub-second DA overflow evoked by single pulses and action potential trains. Unexpectedly, none of the models displayed any dysfunction of DA overflow or reuptake. These results, compatible with the lack of DA neuron loss in these models, suggest that molecular dysfunctions caused by the absence or mutation of these individual genes are not sufficient to perturb the function and survival of mouse DA neurons.
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