PT  - JOURNAL ARTICLE
AU  - Hyo Jung Kang
AU  - David H. Adams
AU  - Arthur Simen
AU  - Birgitte B. Simen
AU  - Grazyna Rajkowska
AU  - Craig A. Stockmeier
AU  - James C. Overholser
AU  - Herbert Y. Meltzer
AU  - George J. Jurjus
AU  - Lisa C. Konick
AU  - Samuel S. Newton
AU  - Ronald S. Duman
TI  - Gene Expression Profiling in Postmortem Prefrontal Cortex of Major Depressive Disorder
AID  - 10.1523/JNEUROSCI.4083-07.2007
DP  - 2007 Nov 28
TA  - The Journal of Neuroscience
PG  - 13329--13340
VI  - 27
IP  - 48
4099  - http://www.jneurosci.org/content/27/48/13329.short
4100  - http://www.jneurosci.org/content/27/48/13329.full
SO  - J. Neurosci.2007 Nov 28; 27
AB  - Investigations of the molecular mechanisms underlying major depressive disorder (MDD) have been hampered by the complexity of brain tissue and sensitivity of gene expression profiling approaches. To address these issues, we used discrete microdissections of postmortem dorsolateral prefrontal cortex (DLPFC) (area 9) and an oligonucleotide (60mer) microarray hybridization procedure that increases sensitivity without RNA amplification. Mixed-effects statistical methods were used to rigorously control for medication usage in the subset of medicated depressed subjects. These analyses yielded a rich profile of dysregulated genes. Two of the most highly dysregulated genes of interest were stresscopin, a neuropeptide involved in stress responses, and Forkhead box D3 (FOXD3), a transcription factor. Secondary cell-based analysis demonstrated that stresscopin and FoxD3 are increased in neurons of DLPFC gray matter of MDD subjects. These findings identify abnormal gene expression in a discrete region of MDD subjects and contribute to further elucidation of the molecular alterations of this complex mood disorder.