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- W2078607645 abstract "In this work, the mechanisms responsible for dopamine (DA) release impairments observed previously in Huntington’s disease model R6/2 mice were evaluated. Voltammetrically measured DA release evoked in striatal brain slices from 12-week old R6/2 mice by a single electrical stimulus pulse was only 19% of wild-type (WT) control mice. Iontophoresis experiments suggest that the concentration of released DA is not diluted by a larger striatal extracellular volume arising from brain atrophy, but, rather, that striatal dopaminergic terminals have a decreased capacity for DA release. This decreased capacity was not due to an altered requirement for extracellular Ca2+, and, as in WT mice, the release in R6/2 mice required functioning vesicular transporters. Catecholamine secretion from individual vesicles was measured during exocytosis from adrenal chromaffin cells harvested from R6/2 and WT mice. While the number of exocytotic events was unchanged, the amounts released per vesicle were significantly diminished in R6/2 mice, indicating that vesicular catecholamines are present in decreased amounts. Treatment of chromaffin cells with 3-nitropropionic acid decreased the vesicular release amount from WT cells by 50%, mimicking the release observed from untreated R6/2 cells. Thus, catecholamine release from tissues isolated from R6/2 mice is diminished because of impaired vesicle loading." @default.
- W2078607645 created "2016-06-24" @default.
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- W2078607645 date "2007-12-01" @default.
- W2078607645 modified "2023-10-10" @default.
- W2078607645 title "Catecholamine exocytosis is diminished in R6/2 Huntington’s disease model mice" @default.
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- W2078607645 doi "https://doi.org/10.1111/j.1471-4159.2007.04908.x" @default.
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