Activation of nicotinic acetylcholine receptors induces long-term potentiation in vivo in the intact mouse dentate gyrus
Activation of nicotinic acetylcholine receptors induces long-term potentiation in vivo in the intact mouse dentate gyrus
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DOI：
10.1046/j.1460-9568.2000.00259.x
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发表时间：
2000-10-01
影响因子：
3.4
通讯作者：
Nishizaki, T
中科院分区：
文献类型：
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作者：
Matsuyama, S;Matsumoto, A;Nishizaki, T
本研究采用细胞外记录技术，探讨烟碱型乙酰胆碱受体（nAChRs）在小鼠齿状回长时程增强（LTP）中的作用。以3.0 mg/kg但不是0.03或0.3 mg/kg剂量腹腔内应用尼古丁产生了与强直性LTP相似的逐渐发展的、持续120 min的长期增加。9.0 mg/kg剂量的尼古丁导致暂时性升高，随后出现抑郁。美加明（0.5 mg/kg ip）预处理可显著抑制烟碱（3.0 mg/kg）诱导的长时程增强（LTPn）和强直性LTP，一种非选择性烟碱拮抗剂，但不受美加明后应用的影响。有趣的是，胆碱，一种选择性α 7 nAChR激动剂，在3.0-90 mg/kg时，在体内以剂量依赖的方式在完整的小鼠齿状回中诱导类似于LTPn的持久增强。胆碱（30 mg/kg i. p.）另外，通过后应用尼古丁（3.0 mg/kg i. p.）或强直刺激。本研究显示，全身应用尼古丁或胆碱在体内诱导了完整小鼠齿状回中的持久增强，表明α 7 nAChR可能有助于尼古丁诱导LTP，并支持体内动物研究，即尼古丁改善学习和记忆表现。
The present study was conducted to clarify the role of nicotinic ACh receptors (nAChRs) on long-term potentiation (LTP) in vivo in the intact mouse dentate gyrus using extracellular recording techniques. Intraperitoneal application of nicotine at a dose of 3.0 mg/kg but not 0.03 or 0.3 mg/kg produced a gradually developing, long-lasting increase for 120 min similar to tetanic LTP. Nicotine at a dose of 9.0 mg/kg caused a temporary increase followed by depression. The long-lasting potentiation induced by nicotine at 3.0 mg/kg, which was named nicotinic long-term potentiation (LTPn), and tetanic LTP were significantly suppressed by pretreatment with mecamylamine (0.5 mg/kg i.p.), a nonselective nicotinic antagonist, but not affected by postapplication of mecamylamine. Interestingly, choline, a selective alpha 7 nAChR agonist, at 3.0-90 mg/kg, induced the long-lasting potentiation similar to LTPn in a dose-dependent manner in vivo in the intact mouse dentate gyrus. The long-lasting potentiation induced by choline (30 mg/kg i.p.) was additionally increased by postapplication of nicotine (3.0 mg/kg i.p.) or tetanic stimulation. The present study revealed that systemic application of nicotine or choline induced the long-lasting potentiation in vivo in the intact mouse dentate gyrus, suggesting that alpha 7 nAChRs may contribute to the induction of LTP by nicotine, and supporting in vivo animal studies that nicotine improves learning and memory performance.