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#kappa#--银环蛇毒素敏感的烟碱受体激活引起的去甲肾上腺素释放参与烟碱诱导的长时程增强样反应

余剑平, 何进, 刘丹, 邓春玉, 朱小南, 汪雪兰, 王勇, 陈汝筑

中山大学中山医学院实验教学中心.广东,广州 510080；中山大学中山医学院药理教研室.广东,广州 510080；广东省人民医院医学研究中心.广东,广州 510080；中山大学药学院药物分析与质量评估实验室.广东,广州 510080；南方医科大学珠江医院临床药理室.广东,广州 510282

摘要

烟碱可以增强学习记忆功能,但其相关机制仍不清楚。海马长时程增强被认为是学习记忆的细胞机制。该研究室以往研究表明,当单脉冲的强度为诱发80%最大群体锋电位时,烟碱(10#mu#mol/L)可以在海马CA1区诱导长时程增强样反应。该文通过细胞外记录离体海马脑片CA1区锥体细胞层群体锋电位,探讨烟碱诱导长时程增强样反应所涉及的烟碱受体亚型与相应的神经递质释放。结果显示,烟碱诱导的长时程增强样反应可以被美加明(mecamylamine,1#mu#mol/L)或#kappa#--银环蛇毒素(#kappa#--bungarotoxin,0.1#mu#mol/L)阻断,但不被dihydro--#beta#--erythtroidine(DHBE,10#mu#mol/L)阻断。烟碱诱导的长时程增强样反应可以被普萘洛尔(propranolol,10#mu#mol/L)阻断,但不被酚妥拉明(phentolamine,10#mu#mol/L)或阿托品(atropine,10#mu#mol/L)阻断。以上结果提示,#kappa#--银环蛇毒素敏感的烟碱受体激活引起的去甲肾上腺素释放参与烟碱诱导的海马CA1区长时程增强样反应。

关键词： 长时程增强; #kappa#-银环蛇毒素; 烟碱受体; 去甲肾上腺素; 海马

Noradrenaline release by activation of #kappa#--bungarotoxin--sensitive nicotinic acetylcholine receptors participates in long--term potentiation--like response induced by nicotine

Yu Jianping, He Jin, Liu Dan, Deng Chunyu, Zhu Xiaonan, Wang Xuelan, Wang Yong, Chen Ruzhu

Experimental Teaching Center,Zhongshan School of Medicine, Sun Yat-Sen University.Guangzhou 510080,Guangdong；China；Research Center of Medical Sciences, Guangdong Provincial People's Hospital.Guangzhou 510080,Guangdong；Depar

Abstract

Nicotine enhances the function of learning and memory, but the underlying mechanism still remains unclear. Hippocampal long-term potentiation （LTP） is assumed to be a cellular mechanism of learning and memory. Our previous experiments showed that with the single pulses evoking 80% of the maximal population spike （PS） amplitude, nicotine （10 #mu#mol/L） induced LTP-like response in the hippocampal CAI region. In the present study, the nicotinic acetylcholine receptor （nAChR） subtypes and relevant neurotransmitter releases involved in LTP-like response induced by nicotine were investigated by extracellularly recording the PS in the pyramidal cell layer in the hippocampal CAI region in vitro. LTP-like response induced by nicotine was blocked by mecamylamine （1 #mu#mol/L） or #kappa#-bungarotoxin （0.1 #mu#mol/L）, but not by dihydro-#beta#-erythtroidine （DH#beta#E, 10 #mu#mol/L）. Moreover, it was inhibited by propranolol （10 #mu#mol/L）, but not by phentolamine （10 #mu#mol/L） or atropine （10 #mu#mol/L）. The results suggest that noradrenaline release secondary to the activation of #beta#-bungarotoxin-sensitive nAChRs participates in LTP-like response induced by nicotine in the hippocampal CAI region.

Key words: Long-term potentiation;#kappa#-bungarotoxin;nicotinic acetylcholine receptors;Noradrenaline;Hippocampus

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引用本文：

余剑平, 何进, 刘丹, 邓春玉, 朱小南, 汪雪兰, 王勇, 陈汝筑. #kappa#--银环蛇毒素敏感的烟碱受体激活引起的去甲肾上腺素释放参与烟碱诱导的长时程增强样反应[J]. 生理学报 2007; 59 (6): 814-820.

Yu Jianping, He Jin, Liu Dan, Deng Chunyu, Zhu Xiaonan, Wang Xuelan, Wang Yong, Chen Ruzhu. Noradrenaline release by activation of #kappa#--bungarotoxin--sensitive nicotinic acetylcholine receptors participates in long--term potentiation--like response induced by nicotine. Acta Physiol Sin 2007; 59 (6): 814-820 (in Chinese with English abstract).