| First Author | Johnson MA | Year | 2007 |
| Journal | J Neurochem | Volume | 103 |
| Issue | 5 | Pages | 2102-10 |
| PubMed ID | 17868298 | Mgi Jnum | J:128746 |
| Mgi Id | MGI:3767932 | Doi | 10.1111/j.1471-4159.2007.04908.x |
| Citation | Johnson MA, et al. (2007) Catecholamine exocytosis is diminished in R6/2 Huntington's disease model mice. J Neurochem 103(5):2102-10 |
| abstractText | 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 Ca(2+), 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. |
