Early attenuation of long-term potentiation in senescence-accelerated mouse prone 8

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• 作者：Sakiko Taniguchi ; Hisato Mizuno ; Masayoshi Kuwahara…
• 关键词：Senescence ; accelerated mouse ; Long ; term potentiation ; Learning and memory ; Aging
• 刊名：Experimental Brain Research
• 出版年：2015
• 出版时间：November 2015
• 年：2015
• 卷：233
• 期：11
• 页码：3145-3152
• 全文大小：653 KB
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• 作者单位：Sakiko Taniguchi (1)
  Hisato Mizuno (1)
  Masayoshi Kuwahara (1)
  Koichi Ito (1)
  
  1. Department of Veterinary Pathophysiology and Animal Health, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, 113-8657, Japan
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Neurology
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1432-1106

文摘

Senescence-accelerated mouse (SAM) is an experimental model animal showing a short lifespan and rapid advancement of senescence. Especially, SAM prone 8 (SAMP8) shows age-related impairment of learning and memory, and thus, it is a good model for age-related cognitive function. However, the synaptic characteristics related to cognitive function of SAMP8 have been poorly understood. In this study, we quantitatively evaluated the synaptic transmission and synaptic plasticity using hippocampal slices obtained from SAMP8 with electrophysiological methods to elucidate the synaptic features of SAMP8. We used the field recordings to measure some synaptic parameters. The slope of field excitatory postsynaptic potentials decreased with age in both SAMP8 and SAM resistant 1 (SAMR1), the control strain of SAMP8. The paired-pulse ratio (PPR), a representative of short-term synaptic plasticity, also decreased in both strains with age. On the other hand, although both SAMR1 and SAMP8 exhibited age-dependent decrease in long-term potentiation (LTP), a representative of long-term synaptic plasticity, the decrease in LTP in SAMP8 started at 6 months of age, while in SAMR1, it was observed at 14 months but not at 6 months of age. The PPRs after high-frequency stimulation for LTP induction were smaller than those before the stimulation. These results indicate that synaptic plasticity in SAMP8 deteriorates at an earlier age compared to SAMR1, and are consistent with behavioral tests showing early impairment of learning and memory of SAMP8. Our study is the first report on quantitative analysis of synaptic function at SAMP8 hippocampus and corroborates the behavioral studies showing cognitive dysfunction with age; therefore, it will be helpful for future studies on aging.