BMC Neuroscience | |
Estradiol prevents olfactory dysfunction induced by A-β 25–35 injection in hippocampus | |
Rosalinda Guevara-Guzmán1  Keith M Kendrick2  Selva Rivas-Arancibia1  Carlos Bernal-Mondragón1  | |
[1] Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México. Apdo, Postal 70250, D.F. México, Delegación Coyoacán 04510, Mexico;Key Laboratory for Neuroinformation, School of Life Science & Technology, University of Electronic Science & Technology of China (UESTC), 610054, Chengdu, P.R. China | |
关键词: Olfactory disfunction; Alzheimer’s disease; Estrogen; Neuroprotection; Neurodegeneration; Amyloid beta; | |
Others : 1140081 DOI : 10.1186/1471-2202-14-104 |
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received in 2013-01-14, accepted in 2013-09-19, 发布年份 2013 | |
【 摘 要 】
Background
Some neurodegenerative diseases, such as Alzheimer and Parkinson, present an olfactory impairment in early stages, and sometimes even before the clinical symptoms begin. In this study, we assess the role of CA1 hippocampus (structure highly affected in Alzheimer disease) subfield in the rats’ olfactory behavior, and the neuroprotective effect of 17 beta estradiol (E2) against the oxidative stress produced by the injection of amyloid beta 25–35.
Results
162 Wistar rats were ovariectomized and two weeks after injected with 2 μl of amyloid beta 25–35 (A-β25–35) in CA1 subfield. Olfactory behavior was evaluated with a social recognition test, odor discrimination, and search tests. Oxidative stress was evaluated with FOX assay and Western Blot against 4-HNE, Fluoro Jade staining was made to quantify degenerated neurons; all these evaluations were performed 24 h, 8 or 15 days after A-β25–35 injection. Three additional groups treated with 17 beta estradiol (E2) were also evaluated. The injection of A-β25–35 produced an olfactory impairment 24 h and 8 days after, whereas a partial recovery of the olfactory behavior was observed at 15 days. A complete prevention of the olfactory impairment was observed with the administration of E2 two weeks before the amyloid injection (A-β25–35 24 h + E2) and one or two weeks after (groups 8 A-β +E2 and 15 A-β +E2 days, respectively); a decrease of the oxidative stress and neurodegeneration were also observed.
Conclusions
Our finding shows that CA1 hippocampus subfield plays an important role in the olfactory behavior of the rat. The oxidative stress generated by the administration of A-β25–35 is enough to produce an olfactory impairment. This can be prevented with the administration of E2 before and after amyloid injection. This suggests a possible therapeutic use of estradiol in Alzheimer’s disease.
【 授权许可】
2013 Bernal-Mondragón et al.; licensee BioMed Central Ltd.
【 预 览 】
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