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加速老化敏感 6 号小鼠(SAMP6)作为脑研究的动物模型的特征。

Characterization of senescence-accelerated mouse prone 6 (SAMP6) as an animal model for brain research.

机构信息

Support Unit for Animal Resources Development, Research Resources Center, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan.

出版信息

Exp Anim. 2014;63(1):1-9. doi: 10.1538/expanim.63.1.

DOI:10.1538/expanim.63.1
PMID:24521858
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4160935/
Abstract

The senescence-accelerated mouse (SAM) was developed by selective breeding of the AKR/J strain, based on a graded score for senescence, which led to the development of both senescence-accelerated prone (SAMP), and senescence-accelerated resistant (SAMR) strains. Among the SAMP strains, SAMP6 is well characterized as a model of senile osteoporosis, but its brain and neuronal functions have not been well studied. We therefore decided to characterize the central nervous system of SAMP6, in combination with different behavioral tests and analysis of its biochemical and pharmacological properties. Multiple behavioral tests revealed higher motor activity, reduced anxiety, anti-depressant activity, motor coordination deficits, and enhanced learning and memory in SAMP6 compared with SAMR1. Biochemical and pharmacological analyses revealed several alterations in the dopamine and serotonin systems, and in long-term potentiation (LTP)-related molecules. In this review, we discuss the possibility of using SAMP6 as a model of brain function.

摘要

加速老化小鼠(SAM)是通过 AKR/J 品系的选择性繁殖培育而成的,其依据的是衰老的分级评分,这导致了加速老化敏感(SAMP)和抗老化(SAMR)品系的发展。在 SAMP 品系中,SAMP6 是一种典型的老年性骨质疏松症模型,但它的大脑和神经元功能尚未得到很好的研究。因此,我们决定对 SAMP6 的中枢神经系统进行特征描述,结合不同的行为测试和对其生化和药理学特性的分析。多项行为测试表明,与 SAMR1 相比,SAMP6 的运动活性更高,焦虑程度更低,抗抑郁活性更强,运动协调能力更差,学习和记忆能力更强。生化和药理学分析揭示了多巴胺和 5-羟色胺系统以及长时程增强(LTP)相关分子的多种改变。在这篇综述中,我们讨论了将 SAMP6 用作大脑功能模型的可能性。

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本文引用的文献

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Cognitive abnormalities and hippocampal alterations in monoamine oxidase A and B knockout mice.单胺氧化酶 A 和 B 基因敲除小鼠的认知异常和海马改变。
Proc Natl Acad Sci U S A. 2013 Jul 30;110(31):12816-21. doi: 10.1073/pnas.1308037110. Epub 2013 Jul 15.
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Does increasing the ratio of AMPA-to-NMDA receptor mediated neurotransmission engender antidepressant action? Studies in the mouse forced swim and tail suspension tests.增加 AMPA 型谷氨酸受体与 NMDA 型谷氨酸受体介导的神经递质传递是否会产生抗抑郁作用?在小鼠强迫游泳和悬尾试验中的研究。
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Amphetamine-induced sensitization has little effect on multiple learning paradigms and fails to rescue mice with a striatal learning defect.安非他命诱导的敏化对多种学习范式影响不大,也不能挽救纹状体学习缺陷的小鼠。
PLoS One. 2013 Apr 15;8(4):e59964. doi: 10.1371/journal.pone.0059964. Print 2013.
4
Serotonin induces long-term depression at corticostriatal synapses.血清素在皮质纹状体突触诱导长时程抑郁。
J Neurosci. 2011 May 18;31(20):7402-11. doi: 10.1523/JNEUROSCI.6250-10.2011.
5
Hallucinogenic 5-hydroxytryptamine 2A receptor agonist effects in senescence-accelerated mice.致幻 5-羟色胺 2A 受体激动剂对快速老化小鼠的影响。
Exp Anim. 2010;59(4):441-7. doi: 10.1538/expanim.59.441.
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Quantitative trait locus on chromosome X affects bone loss after maturation in mice.X 染色体上的数量性状位点影响小鼠成熟后的骨质流失。
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Exp Gerontol. 2008 Sep;43(9):847-52. doi: 10.1016/j.exger.2008.06.010. Epub 2008 Jul 4.