Journal
BRAIN RESEARCH
Volume 1059, Issue 1, Pages 7-12Publisher
ELSEVIER
DOI: 10.1016/j.brainres.2005.08.004
Keywords
R406W human tau; transgenic mouse; depression; 5-hydroxytryptamine (5-HT); Alzheimer's disease; frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17)
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Mutant R406W human tau was originally identified in frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) and causes a hereditary tauopathy that clinically resembles Alzheimer's disease (AD). In the current study, we examined the performance of R406W transgenic (Tg) mice in the forced swimming test, a test with high predictivity of antidepressant efficacy in human depression, and found an enhancement of the immobility time. In contrast, the motor function and anxiety-related emotional response of R406W Tg mice were normal. Furthermore, a selective serotonin reuptake inhibitor (SSR1), fluvoxamine (100 mg/ka, p.o.), significantly reduced this enhancement of the immobility time, whereas a noradrenaline reuptake inhibitor, desipramine, had no effect. In an in vivo microdialysis study, R406W Tg mice exhibited a significantly decreased extracellular 5-hydroxyindoleacetic acid (5-HIAA) level in the frontal cortex and also exhibited a tendency toward a decreased extracellular 5-hydroxytryptamine (5-HT) level. Moreover, fluvoxamine, which reduced the enhancement of the immobility time, significantly increased the extracellular 5-HT level in R406W Tg mice. These results suggest that R406W Tg mice exhibit changes in depress ion-related behavior involving serotonergic neurons and provide an animal model for investigating AD with depression. (c) 2005 Elsevier B.V All rights reserved.
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