κ-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(英文)

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

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。本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(10μmol/L)可以在海马CA1区诱导长时程增强样反应。本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,1μmol/L)或κ-银环蛇毒素(κ- bungarotoxin,0.1μmol/L)阻断,但不被dihydro-β-erythtroidine(DHBE,10μmol/L)阻断。烟碱诱导的长时程增强样反应可以被普萘洛尔(propranolol,10μmol/L)阻断,但不被酚妥拉明(phentolamine,10μmol/L)或阿托品(atropine,10μmol/L)阻断。以上结果提示,κ-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。

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 μmol/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 μmol/L） or k-bungarotoxin （0.1 μmol/L）, but not by dihydro-β-erythtroidine （DHβE, 10 μmol/L）. Moreover, it was inhibited by propranolol （10 μmol/L）, but not by phentolamine （10 μmol/L） or atropine （10 μmol/L）. The results suggest that noradrenaline release secondary to the activation of β-bungarotoxin-sensitive nAChRs participates in LTP-like response induced by nicotine in the hippocampal CAI region.