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大鼠海马CA1区β2肾上腺素能受体激活抑制晚期相长时程增强

β2-Adrenergic Activation Inhibits Long-term Potentiation of Field Excitatory Postsynaptic Potentials in the Hippocampal CA1 Region of Rats

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【作者】 朱壁李葆明

【Author】 ZHU Bi,LI Bao-ming(Institute of Neurobiology,Institutes of Brain Science,Fudan University,Shanghai 200032,China)

【机构】 复旦大学脑科学研究院神经生物学研究所脑高级功能实验室

【摘要】 海马在陈述性学习和记忆中起关键作用,海马内长时程增强(long-term potentiation,LTP)被认为是学习和记忆的突触机制.β肾上腺素能受体(β-受体)在海马中大量分布.实验室先前工作表明,在CA1和CA3区,β1受体和β2受体有不同的亚细胞分布.大量的研究工作证实了β1受体在LTP中的重要作用,而关于β2受体在LTP中的作用所知甚少.研究应用在体场电位记录方法,研究β2受体激活对CA1区LTP的影响.实验结果表明,CA1区内给予β2受体激动剂Clenbuterol(10 ng)能显著抑制晚期相LTP,但对早期相LTP没有显著效应;Clenbuterol对晚期相LTP的抑制效应能被β2受体拮抗剂ICI 118551所逆转.这些结果提示,海马CA1区内β2受体的激活抑制晚期相LTP的维持.

【Abstract】 The hippocampus plays a critical role in learning and memory.Long-term potentiation(LTP) of synaptic transmission in the hippocampus is regarded as a synaptic mechanism for learning and memory.(β-Adrenoceptors,β-ARs) are widely distributed in the hippocampus.Previous study in our laboratory has shown that,in the CA1 and CA3 regions,β1-and β2-ARs have differential sub-cellular localizations.While much is known about the importance of β1-AR for LTP,the role of β2-AR is largely unclear.Here,the regulation by β2-AR of LTP in the CA1 region was investigated,using in vivo field potential recording.The results showed that intra-CA1 infusion of the β2-AR agonist Clenbuterol(10 ng) significantly inhibited late-phase LTP(L-LTP),whereas early-phase LTP(E-LTP) was intact.This inhibitory effect no longer existed in the presence of the β2-AR antagonist ICI 118551.These results suggest that β2-AR might play a negative regulation on L-LTP in the CA1 region.

  • 【文献出处】 复旦学报(自然科学版) ,Journal of Fudan University(Natural Science) , 编辑部邮箱 ,2009年03期
  • 【分类号】Q42
  • 【下载频次】136
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