Kudo Y, Ogura A, Iijima T
Department of Neuroscience, Mitsubishi-Kasei Institute of Life Sciences, Tokyo, Japan.
Neurosci Lett. 1988 Mar 10;85(3):345-50. doi: 10.1016/0304-3940(88)90590-3.
Changes in cytosolic free Ca2+ concentration ([Ca2+]i) in response to acetylcholine (ACh) were examined by fura-2 fluorometry in cultured rat hippocampal neurons. ACh (greater than or equal to 10(-5) M) induced an increase in [Ca2+]i composed of fast transient and slow long-lasting phases. Atropine (10(-8) M) abolished the fast component and greatly reduced the slow component. The slow component was selectively blocked by pirenzepine (10(-6) M). The effect of ACh remained partially in a Ca2+-deficient medium where effects of L-glutamate and KCl (50 mM) were abolished. Present results suggest that ACh elevates [Ca2+]i by activation of muscarinic receptor subtypes, one of which is coupled with ion channels and the other of which transduces the ACh binding to mobilization of intracellularly stored Ca2+.
采用fura-2荧光测定法检测了培养的大鼠海马神经元中胞质游离钙离子浓度（[Ca2+]i）对乙酰胆碱（ACh）的反应。ACh（大于或等于10(-5) M）诱导[Ca2+]i升高，包括快速瞬变和缓慢持久两个阶段。阿托品（10(-8) M）消除了快速成分并大大降低了缓慢成分。缓慢成分被哌仑西平（10(-6) M）选择性阻断。在缺乏钙离子的培养基中，ACh的作用仍部分存在，而L-谷氨酸和氯化钾（50 mM）的作用则被消除。目前的结果表明，ACh通过激活毒蕈碱受体亚型来升高[Ca2+]i，其中一种与离子通道偶联，另一种将ACh结合转化为细胞内储存钙离子的动员。
