Journal
JOURNAL OF NEUROSCIENCE
Volume 27, Issue 48, Pages 13329-13340Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4083-07.2007
Keywords
microarray; stresscopin; urocortin III; stress; corticotrophin releasing hormone; FoxD3; fibroblast growth factor
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Funding
- NCRR NIH HHS [P20 RR017701-076630, P20 RR017701-076632, S10 RR019895, 1KL2RR024138, RR19895-02, P20 RR017701, RR17701, S10 RR019895-010002, KL2 RR024138] Funding Source: Medline
- NIMH NIH HHS [R37 MH045481, MH61578, P50 MH060451-080002, P01 MH025642-30, MH67996, P01 MH025642, MH25642, MH60451, P50 MH060451, R01 MH061578, R01 MH045481-13, MH45481, R01 MH067996, R01 MH061578-02, R01 MH045481, R01 MH067996-03S1] Funding Source: Medline
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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.
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