Expression analysis for inverted effects of serotonin transporter inactivation

Inactivation of serotonin transporter (HTT) by pharmacologically in the neonate or genetically increases risk for depression in adulthood, whereas pharmacological inhibition of HTT ameliorates symptoms in depressed patients. The differing role of HTT function during early development and in adult br...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2008-03, Vol.368 (1), p.43-49
Main Authors: Ichikawa, Manabu, Okamura-Oho, Yuko, Shimokawa, Kazuro, Kondo, Shinji, Nakamura, Sakiko, Yokota, Hideo, Himeno, Ryutaro, Lesch, Klaus-Peter, Hayashizaki, Yoshihide
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Animals
BRAIN
CELL PROLIFERATION
Depression
Gene Expression Profiling
Gene Expression Regulation - genetics
Gene knockout
GENE REGULATION
GENES
KNOCK-OUT REACTIONS
MICE
Mice, Knockout
Model mouse
NEONATES
NERVE CELLS
Oligonucleotide Array Sequence Analysis
RNA, Messenger - genetics
SEROTONIN
Serotonin Plasma Membrane Transport Proteins - deficiency
Serotonin Plasma Membrane Transport Proteins - genetics
Serotonin Plasma Membrane Transport Proteins - metabolism
Serotonin transporter
Transcriptional regulation
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Summary:Inactivation of serotonin transporter (HTT) by pharmacologically in the neonate or genetically increases risk for depression in adulthood, whereas pharmacological inhibition of HTT ameliorates symptoms in depressed patients. The differing role of HTT function during early development and in adult brain plasticity in causing or reversing depression remains an unexplained paradox. To address this we profiled the gene expression of adult Htt knockout (Htt KO) mice and HTT inhibitor-treated mice. Inverted profile changes between the two experimental conditions were seen in 30 genes. Consistent results of the upstream regulatory element search and the co-localization search of these genes indicated that the regulation may be executed by Pax5, Pax7 and Gata3, known to be involved in the survival, proliferation, and migration of serotonergic neurons in the developing brain, and these factors are supposed to keep functioning to regulate downstream genes related to serotonin system in the adult brain.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2008.01.041