QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rebec, G. V. Articles by Ennis, M. D. Search for Related Content PubMed PubMed Citation Articles by Rebec, G. V. Articles by Ennis, M. D.

 Previous Article  |  Next Article 

The Journal of Neuroscience, 2002, 22:RC202:1-5

RAPID COMMUNICATION
Dysregulation of Ascorbate Release in the Striatum of Behaving Mice Expressing the Huntington's Disease Gene

George V. Rebec, Scott J. Barton, and Michelle D. Ennis

Program in Neural Science, Department of Psychology, Indiana University, Bloomington, Indiana 47405-7007

The extracellular fluid of the striatum contains a high level of ascorbate, an antioxidant vitamin known to play a key role in behavioral activation. We assessed the extracellular dynamics of ascorbate in R6/2 mice engineered to express the gene for Huntington's disease (HD), an autosomal dominant condition characterized by the loss of striatal neurons. Slow-scan voltammetry was used to measure striatal ascorbate during anesthesia and subsequent behavioral recovery. Although both the HD mice and their littermate controls had comparable ascorbate levels during anesthesia, the gradual return of behavioral activation over the next 120 min led to dramatically different ascorbate responses: a progressive increase in controls and a 25-50% decline in HD mice. In contrast, 3,4-dihydroxyphenylacetic acid, a major dopamine metabolite, showed no group differences. Behaviorally, HD mice were less active overall than controls and showed a relatively restricted range of spontaneous movements. Both the ascorbate and behavioral deficits were evident in 6-week-old HD mice and persisted in all subsequent test sessions through 10 weeks of age. Collectively, although these results are consistent with inadequate antioxidant protection in the HD striatum, they indicate that the ascorbate deficit is confined to periods of behavioral activation.

Key words: ascorbate; basal ganglia; dopamine; glutamate; Huntington's disease; motor control; striatum; voltammetry

---

Copyright © Society for Neuroscience  0270-6474//$05.00/0

This article has been cited by other articles:

				A. G. Walker, B. R. Miller, J. N. Fritsch, S. J. Barton, and G. V. Rebec Altered Information Processing in the Prefrontal Cortex of Huntington's Disease Mouse Models J. Neurosci., September 3, 2008; 28(36): 8973 - 8982. [Abstract] [Full Text] [PDF]

				C. Cepeda, R. S. Hurst, C. R. Calvert, E. Hernandez-Echeagaray, O. K. Nguyen, E. Jocoy, L. J. Christian, M. A. Ariano, and M. S. Levine Transient and Progressive Electrophysiological Alterations in the Corticostriatal Pathway in a Mouse Model of Huntington's Disease J. Neurosci., February 1, 2003; 23(3): 961 - 969. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help