期刊文献+

快速老化小鼠海马脑片CA1区神经元放电特征模式研究 被引量:2

Characteristic pattern of neuron firings at hippocampus CA1 for fast-aging mouse
原文传递
导出
摘要 目的研究快速老化对记忆脑区海马CA1神经元电活动兴奋性的影响。方法应用脑片和细胞外记录技术,记录快速老化(sAM.P/8)组和正常对照组小鼠在海马脑片CA1区的锥体神经元自发放电序列,通过计算2组神经元自发放电频率和神经元放电间隔(ISI)研究快速老化对海马CA1区神经元兴奋性的影响。结果快速老化组小鼠海马CA1区神经元自发放电频率为(1.052±0.364)Hz(样本数n1=14),正常对照组为4.416+1.306Hz(样本数n1=22),前者比后者显著降低(P〈0.05);快速老化组ISI≥1s,占80.5%,正常对照组ISI均≤1S,其中95.6%≤0.5S,前者比后者显著延长。结论快速老化组小鼠海马脑片CA1区神经元的发放频率降低,ISI延长。提示快速老化对小鼠海马区神经元兴奋性电活动起到了明显的抑制作用。 Objective To investigate the effect of fast-aging on the excitability of hippocampus CA1 neurons in mouse and the possible interaction between fast-aging and hippocampus. Methods Using brain slice and extraeellular recording technique to record the firing of hippocampus CA 1 neurons in fast-aging(SAM-P/8) and normal control mice, after preprocessing, neural firing train were obtained. Using neural firing rate and inter- spike-inter to investigate interaction between fast-aging and hippocampal neural firing. Results The neural firing rate of hippocampus CAI neurons in fast-aging mice is (1.052_+0.364) Hz(n=14), while the neural firing rate in normal control mice is (4.416±1.306) Hz(n=22). In fast-aging mice, 80.5% inter spike intervel(ISI) is longer than lsec, but in normal control mice, 95.6% ISI is shorter than 0.Ssee. Conclusion The decreased firing rate of hippocampus CA1 and longer ISI observed in the fast-aging mice indicates that fast-aging significantly inhibit hippocampal CA1 neurons excitability.
出处 《国际生物医学工程杂志》 CAS 北大核心 2010年第1期24-26,30,共4页 International Journal of Biomedical Engineering
基金 基金项目:国家自然科学基金资助项目(30770545)
关键词 快速老化 SAM—P/8小鼠 海马脑片 CAl区 自发放电频率 Fast aging SAM-P/8 mouse Hippocampus slice CA1 Firing-rate
  • 相关文献

参考文献10

  • 1Janus C,Westaway D.Transgenic mouse models of Alzheimer's disease[J].Physiol Behav,2001,73(5):873-886.
  • 2Zhang Li-hong,Li Qi,Wolff LT,et al.Changes of brain activity in the aged SA MP mouse[J].Biogerontology,2007,8(2):81-88.
  • 3Pang KCH,Miller JP,Fortress A,et al.Age-related disruptions of circadian rhythm and memory in the senescence-accelerated mouse (SAMP8)[J].Age,2006,28(3):283-296.
  • 4Varona P,Ibarz JM,Lopez-Aguado L,et al.Macroscopic and subcellular factors shaping population spikes[J].J Neurophysiol,2000,83 (4):2192-2208.
  • 5Mattia D,Kawasaki H,Avoli M.In vitro electrophysiology of rat subicular bursting neurons[J].Hippocampus,1997,7(1):48-57.
  • 6Khaliq ZM,Raman IM.Axonal propagation of simple and complex spikes in cerebellar Purkinje neurons[J].J Neurosci,2005,25(2):454-463.
  • 7Price DL,Sisodia SS,Borchelt DR.Genetic neurodegenerative diseases:the human illness and transgenic models[J].Science,1998,282(5391):1079-1083.
  • 8Petkova AT,Leapman RD,Guo Zhi-hong,et al.Self-propagating,molecular-level polymorphism in Alzheimer's beta-amyloid fibrils[J].Science,2005,307(5707):262-265.
  • 9Kayed R,Head E,Thompson JL,et al.Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis[J].Science,2003,300(5618):486-489.
  • 10Brown EN,Kaas RE,Mitts PP.Multiple neural spike train data analysis:state-of-the-art and future challenges[J].Nat Neurosci,2004,7(5):456-461.

同被引文献10

引证文献2

二级引证文献11

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部