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

作　　者：朱壁[1] 李葆明[1] 

机构地区：[1]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,上海200032

出　　处：《复旦学报（自然科学版）》2009年第3期397-401,共5页Journal of Fudan University：Natural Science

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.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.

关 键 词：海马 Β2肾上腺素能受体 长时程增强 大鼠 

分 类 号：Q427[生物学—神经生物学]