Volume 7 Supplement 1

Proceedings of the 2011 International Conference on Molecular Neurodegeneration

Open Access

Gastrodin improves learning behavior in a rat model of Alzheimer's disease induced by intra-hippocampal Aβ 1-40 injection

Molecular Neurodegeneration20127(Suppl 1):S15

https://doi.org/10.1186/1750-1326-7-S1-S15

Published: 7 February 2012

Background

Gastrodin extracted from the rhizome of Gastrodia elata Blume, a Chinese herbal medicine, has long been used for treating vertigo, general paralysis, epilepsy, tetanus, stroke and dementia. Although several reports have shown that gastrodin has neuroprotective effects to rescue lead-induced synaptic plasticity deficits in rat hippocampus, and hippocampal cell damage in cellular model of Alzheimer’s disease induced by Aβ25-35, its effect on behaviors of rat model of Alzheimer's disease induced by intra-hippocampal Aβ injection is not studied yet.

Methods

Forty-one male adult Sprague–Dawley rats were randomly divided into groups: normal (n=10), sham operated (n=7, intra-hippocampal saline injection), saline (n=8, intra-hippocampal Aβ injection and then ig saline), gastrodin (n=8, intra-hippocampal Aβ injection and then ig gastrodin), huperzine A (n=8, intra-hippocampal Aβ injection and then ig huperzine A). One week after intra-hippocampal Aβ1-40 injection (5 μg in 1 μl PBS, bilaterally), gastrodin (200 mg/kg), huperzine A (300 μg/kg) or saline were administrated by ig for 27 days (q.d.). At end of gastrodin or huperzine A treatment, the 5-day Morris water maze test was performed to observe the learning and memory function of 5 groups of animals.

Results

Two-way ANOVA (repeated measures) was used to compare the difference of escape latency in place navigation trials among testing days or groups, and showed both differences among 5 test days and 5 groups were very significant (P<0.001). Bonferroni posttests indicated that the difference between normal and sham operated was not significant (P>0.05), but the latency in saline group was significantly longer than normal or sham operated groups (P<0.05 or P<0.01), suggesting establishment of rat model. Compared to other groups, the latency in gastrodin group at 2nd test day was significantly shorter than saline group (P<0.05), indicating learning improvement of rat model. However, the latency in huperzine A group was observed to be longer than normal group (P<0.01). In spatial probe trial after 5-day place navigation trials, difference of numbers to cross the assumed platform among 5 groups was not significant (One-way ANOVA, P>0.05).

Conclusion

Gastrodin may have therapeutic effect to improve learning behavior in rat model of Alzheimer's disease induced by intra-hippocampal Aβ1-40 injection by mechanism different from huperzine A.

Declarations

Acknowledgements

This work was supported by the NSF of Anhui Province, China (090413084).

Authors’ Affiliations

(1)
Cell Electrophysiology Laboratory, Wannan Medical College

Copyright

© Liu and Wang; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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