期刊
CELL DEATH & DISEASE
卷 2, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/cddis.2011.79
关键词
Alzheimer's disease; serotonin; serotonin transporter; electron microscopy; hippocampus; plasticity
类别
资金
- Alzheimer's Research Trust [ART/PG2004A/1]
- Government of the Basque Country [AE-2010-1-28, AEGV10/16]
- BBSRC
Alzheimer's disease (AD) is a neurodegenerative pathology that deteriorates mnesic functions and associated brain regions including the hippocampus. Serotonin (5-HT) has an important role in cognition. We recently demonstrated an increase in 5-HT transporter (SERT) fibre density in the hippocampal CA1 in an AD triple transgenic mouse model (3xTg-AD). Here, we analyse the ultrastructural localisation, distribution and numerical density (N(v)) of hippocampal SERT axons (SERT-Ax) and terminals (SERT-Te) and their relationship with SERT fibre sprouting and altered synaptic N(v) in 3xTg-AD compared with non-transgenic control mice. 3xTg-AD animals showed a significant increase in SERT-Te N(v) in CA1 at both, 3 (95%) and 18 months of age (144%), being restricted to the CA1 stratum moleculare (S. Mol; 227% at 3 and 180% at 18 months). 3xTg-AD animals also exhibit reduced N(v) of perforated axospinous synapses (PS) in CA1 S. Mol (56% at 3 and 52% at 18 months). No changes were observed in the N(v) of symmetric and asymmetrical synapses or SERT-Ax. Our results suggest that concomitant SERT-Te N(v) increase and PS reduction in 3xTg-AD mice may act as a compensatory mechanism maintaining synaptic efficacy as a response to the AD cognitive impairment. Cell Death and Disease (2011) 2, e210; doi:10.1038/cddis.2011.79; published online 15 September 2011
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