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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 can enhance learning and memory function, but its relevant mechanism remains unclear. Long-term potentiation of the hippocampus is considered to be the cellular mechanism for learning and memory. Previous studies in our laboratory have shown that nicotine (10 μmol/L) induces long-term potentiation-like responses in the CA1 region of the hippocampus when the intensity of a single pulse is 80% of the maximum population spike. In this study, the nicotine receptor subtypes and corresponding neurotransmitter release involved in nicotine-induced long-term potentiation-like responses were investigated by extracellular recording of the spikes in the pyramidal cell layer in the hippocampal CA1 region. The results showed that nicotine-induced long-term potentiation-like responses could be blocked by mecamylamine (1 μmol/L) or κ-bungarotoxin (0.1 μmol/L) but not by dihydro-β -erythtroidine (DHBE, 10 μmol/L) blocked. Nicotine-induced long-term potentiation-like responses can be blocked by propranolol (10 μmol/L) but not phentolamine (10 μmol/L) or atropine (10 μmol/L). Broken. These results suggest that norepinephrine release induced by activation of kappa-bungarotoxin-sensitive nicotinic receptors participates in the long-term potentiation-like response in the nicotine-induced hippocampal CA1 region.