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Significant modulation of mitochondrial electron transport system by nicotine in various rat brain regions.

Authors: Wang, J  Kim, JM  Donovan, DM  Becker, KG  Li, MD 
Citation: Wang J, etal., Mitochondrion. 2009 Jun;9(3):186-95. Epub 2009 Jan 30.
Pubmed: (View Article at PubMed) PMID:19460297
DOI: Full-text: DOI:10.1016/j.mito.2009.01.008

The mitochondrion is the organelle responsible for generation of most usable energy in a cell. It also plays an important role in a series of physiological processes such as apoptosis and proliferation. Although previous studies have demonstrated that nicotine modulates the morphology and function of mitochondria, the mechanism(s) underlying these effects is largely unknown. In this study, using a microarray consisting of 4793 clones derived from a mouse dopamine cDNA library, we profiled the gene expression patterns for six brain regions (amygdala, hippocampus, nucleus accumbens, prefrontal cortex, striatum and ventral tegmental area) of female Sprague-Dawley rats subjected to nicotine treatment for 7days through osmotic minipump infusion. We identified a number of genes and pathways, including components of the electron transport system of mitochondria, such as cytochrome c oxidase subunit I (Mt-co1), Mt-co2, Mt-co3, cytochrome b (Mt-cyb), mitochondrial NADH dehydrogenase 4 (Mt-nd4), and Mt-nd6, that were significantly modulated by nicotine in multiple brain regions. Bioinformatics analysis provided evidence that Gene Ontology categories related to the electron transport system were overrepresented in each brain region. Finally, the results from the microarray analysis were verified by quantitative RT-PCR for four representative genes. Together, our findings imply that mitochondria are involved in neuronal adaptation to chronic nicotine exposure.

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CRRD Object Information
CRRD ID: 5507828
Created: 2011-10-04
Species: All species
Last Modified: 2011-10-04
Status: ACTIVE



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