Striatal dopamine transmission is subtly modified in human A53Tα-synuclein overexpressing mice.

PloS One
Nicola J PlattStephanie J Cragg

Abstract

Mutations in, or elevated dosage of, SNCA, the gene for α-synuclein (α-syn), cause familial Parkinson's disease (PD). Mouse lines overexpressing the mutant human A53Tα-syn may represent a model of early PD. They display progressive motor deficits, abnormal cellular accumulation of α-syn, and deficits in dopamine-dependent corticostriatal plasticity, which, in the absence of overt nigrostriatal degeneration, suggest there are age-related deficits in striatal dopamine (DA) signalling. In addition A53Tα-syn overexpression in cultured rodent neurons has been reported to inhibit transmitter release. Therefore here we have characterized for the first time DA release in the striatum of mice overexpressing human A53Tα-syn, and explored whether A53Tα-syn overexpression causes deficits in the release of DA. We used fast-scan cyclic voltammetry to detect DA release at carbon-fibre microelectrodes in acute striatal slices from two different lines of A53Tα-syn-overexpressing mice, at up to 24 months. In A53Tα-syn overexpressors, mean DA release evoked by a single stimulus pulse was not different from wild-types, in either dorsal striatum or nucleus accumbens. However the frequency responsiveness of DA release was slightly modified in A53Tα-...Continue Reading

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Citations

Jan 22, 2013·Bioanalysis·Michael A Johnson
Feb 3, 2015·Trends in Neurosciences·Benjamin H M HunnRichard Wade-Martins
May 4, 2016·Basal Ganglia·David SulzerMargaret E Rice
Sep 26, 2015·Journal of Parkinson's Disease·Nadine BrehmGeorg Auburger
Jan 3, 2015·Neurobiology of Aging·Wei XuJin-Tai Yu
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Oct 10, 2014·Human Molecular Genetics·Suzana GispertGeorg Auburger
Jul 28, 2017·Nature Reviews. Neuroscience·James B KoprichJonathan M Brotchie
Jun 6, 2018·International Journal of Molecular Sciences·Martina PfefferCharlotte von Gall

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