JN Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


J Neurophysiol (December 29, 2004). doi:10.1152/jn.00791.2004
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
93/5/2565    most recent
00791.2004v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ariano, M. A.
Right arrow Articles by Levine, M. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ariano, M. A.
Right arrow Articles by Levine, M. S.
Submitted on August 4, 2004
Accepted on December 23, 2004

Striatal Potassium Channel Dysfunction in Huntington's Disease Transgenic Mice

Marjorie A. Ariano1, Carlos Cepeda2*, Christopher R. Calvert2, Jorge Flores-Hernandez2, Elizabeth Hernandez-Echeagaray2, Gloria J. Klapstein2, Scott H. Chandler3, Neil Aronin4, Marian DiFiglia5, and Michael S. Levine2

1 Mental Retardation Research Center, UCLA, Los Angeles, CA, USA; Department of Neuroscience, The Chicago Medical School, Chicago, IL, USA
2 Mental Retardation Research Center, UCLA, Los Angeles, CA, USA
3 Department of Physiological Sciences, UCLA, Los Angeles, CA, USA
4 Department of Medicine, Massachusetts Medical Center, Worcester, MA, USA
5 Department of Neurology, Massachusetts General Hospital, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: ccepeda{at}mednet.ucla.edu.

Huntington's disease (HD) is a neurodegenerative disorder that mainly affects the projection neurons of the striatum and cerebral cortex. Genetic mouse models of HD have shown that neurons susceptible to the mutation exhibit morphological and electrophysiological dysfunctions before and during development of the behavioral phenotype. We used HD transgenic mouse models to examine inwardly and outwardly rectifying K+ conductances, as well as expression of some related K+ channel subunits. Experiments were conducted in slices and dissociated cells from two mouse models, the R6/2 and TgCAG100, at the beginning and after full development of overt behavioral phenotypes. Striatal medium-sized spiny neurons (MSNs) from symptomatic transgenic mice had increased input resistances, depolarized resting membrane potentials, and reductions in both inwardly and outwardly rectifying K+ currents. These changes were more dramatic in the R6/2 model than in the TgCAG100. Parallel immunofluorescence studies detected decreases in the expression of K+ channel subunit proteins, Kir2.1, Kir2.3 and Kv2.1 in MSNs, which contribute to the formation of the channel ionophores for these currents. Attenuation in K+ conductances and channel subunit expression contribute to altered electrophysiological properties of MSNs and may partially account for selective cellular vulnerability in the striatum.




This article has been cited by other articles:


Home page
J. Neurosci.Home page
S.-Y. Chou, J.-Y. Weng, H.-L. Lai, F. Liao, S. H. Sun, P.-H. Tu, D. W. Dickson, and Y. Chern
Expanded-Polyglutamine Huntingtin Protein Suppresses the Secretion and Production of a Chemokine (CCL5/RANTES) by Astrocytes
J. Neurosci., March 26, 2008; 28(13): 3277 - 3290.
[Abstract] [Full Text] [PDF]


Home page
Hum Mol GenetHome page
D. M. Cummings, A. J. Milnerwood, G. M. Dallerac, V. Waights, J. Y. Brown, S. C. Vatsavayai, M. C. Hirst, and K. P.S.J. Murphy
Aberrant cortical synaptic plasticity and dopaminergic dysfunction in a mouse model of huntington's disease
Hum. Mol. Genet., October 1, 2006; 15(19): 2856 - 2868.
[Abstract] [Full Text] [PDF]


Home page
Hum Mol GenetHome page
A. J. Milnerwood, D. M. Cummings, G. M. Dallerac, J. Y. Brown, S. C. Vatsavayai, M. C. Hirst, P. Rezaie, and K. P.S.J. Murphy
Early development of aberrant synaptic plasticity in a mouse model of Huntington's disease
Hum. Mol. Genet., May 15, 2006; 15(10): 1690 - 1703.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2004 by the The American Physiological Society.