Catecholamine exocytosis is diminished in R6/2 Huntington's disease model mice

Michael A. Johnson, Melissa Villanueva, Christy L. Haynes, Andrew T. Seipel, Leah A. Buhler, R. Mark Wightman

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)2102-2110
Number of pages9
JournalJournal of Neurochemistry
Issue number5
StatePublished - Dec 2007


  • Adrenal chromaffin cells
  • Catecholamine
  • Caudate putamen
  • Cyclic voltammetry
  • Dopamine
  • Huntington's disease


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