WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience
QUICK SEARCH:   [advanced]


     
-


HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP
The Journal of Neuroscience, December 20, 2006, 26(51):13123-13127; doi:10.1523/JNEUROSCI.4191-06.2006

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit an eLetter
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Related articles in J. Neurosci.
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Web of Science (6)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chandrasekaran, K.
Right arrow Articles by Kristian, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chandrasekaran, K.
Right arrow Articles by Kristian, T.

 Previous Article  |  Next Article 

Brief Communications
Neuron-Specific Conditional Expression of a Mitochondrially Targeted Fluorescent Protein in Mice

Krish Chandrasekaran, Julie L. Hazelton, Yu Wang, Gary Fiskum, and Tibor Kristian

Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland 21201

Correspondence should be addressed to either Krish Chandrasekaran or Tibor Kristian, Medical School Teaching Facility 5-34, 685 West Baltimore Street, Baltimore, MD 21201. Email: kchan004{at}umaryland.edu or Email: tkris001{at}umaryland.edu

Mitochondrial dysfunction contributes to the pathophysiology of both acute and chronic neurodegenerative disorders. Quantification of mitochondrial bioenergetic properties generally requires the use of isolated brain mitochondria. However, the involvement of neuronal mitochondrial dysfunction in these disorders is limited by the lack of markers, and therefore isolation procedures, that distinguish neuronal compared with astrocyte mitochondria. To address this and other issues concerning neuronal mitochondria in the CNS, transgenic mice were generated that express a fluorescent protein targeted specifically to neurons. A neuron-specific promoter, CaMKII{alpha} (calcium/calmodulin-dependent kinase II{alpha}) driven tTA (tetracycline transactivator) mice were crossed with TRE (tetracycline responsive element) driven mitochondrial targeted enhanced yellow fluorescent protein (eYFP) mice. Expression of eYFP in the bigenic mouse brain was observed only in neuronal mitochondria of striatum, forebrain, and hippocampus and was enhanced by the removal of the tetracycline analog doxycycline (Dox) in the diet. The respiratory control ratio of synaptic and nonsynaptic mitochondria isolated from eYFP-expressing mice was the same as control mice, suggesting that neuronal mitochondria expressing eYFP maintain normal bioenergetic functions. More importantly, the development of Dox-inducible, neuron targeted mito/eYFP transgenic mice offer a unique in vivo model for delineating the participation of neuronal mitochondria in neuronal survival and death.

Key words: cortex; hippocampus; neuron; mitochondria; transgenic; mice; eYFP; tetracycline; respiration; neurodegeneration; energy metabolism

Received Sept. 25, 2006; revised Nov. 14, 2006; accepted Nov. 14, 2006.

Correspondence should be addressed to either Krish Chandrasekaran or Tibor Kristian, Medical School Teaching Facility 5-34, 685 West Baltimore Street, Baltimore, MD 21201. Email: kchan004{at}umaryland.edu or Email: tkris001{at}umaryland.edu


Related articles in J. Neurosci.:

This Week in The Journal

J. Neurosci. 2006 26: i. [Full Text]  





-
-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help
-
Copyright 2009 by Society for Neuroscience ONLINE ISSN: 1529-2401
-