Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2199091 | Molecular and Cellular Neuroscience | 2008 | 6 Pages |
LRRK2, α-synuclein, UCH-L1 and DJ-1 are implicated in the etiology of Parkinson's disease. We show for the first time that increase in striatal α-synuclein levels induce increased Lrrk2 mRNA levels while Dj-1 and Uch-L1 are unchanged. We also demonstrate that a mouse strain lacking the dopamine signaling molecule DARPP-32 has significantly reduced levels of both Lrrk2 and α-synuclein, while mice carrying a disabling mutation of the DARPP-32 phosphorylation site T34A or lack α-synuclein do not show any changes. To test if striatal dopamine depletion influences Lrrk2 or α-synuclein expression, we used the neurotoxin 6-hydroxydopamine in rats and MitoPark mice in which there is progressive degeneration of dopamine neurons. Because striatal Lrrk2 and α-synuclein levels were not changed by dopamine depletion, we conclude that Lrrk2 and α-synuclein mRNA levels are possibly co-regulated, but they are not influenced by striatal dopamine levels.