Release of non-neuronal acetylcholine from the human placenta: difference to neuronal acetylcholine

Release of non-neuronal acetylcholine from the human placenta: difference to neuronal acetylcholine
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人胎盘释放非神经元乙酰胆碱:与神经元乙酰胆碱的差异

DOI:
10.1007/s002100100445
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发表时间:
2001
期刊:
Naunyn-Schmiedeberg's Archives of Pharmacology
影响因子:
--
通讯作者:
H. Kilbinger
H. Kilbinger
中科院分区:
--
文献类型:
--
作者:
I. Wessler;E. Roth;S. Schwarze;W. Weikel;F. Bittinger;C. Kirkpatrick;H. Kilbinger

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抽象的。研究了人胎盘中广泛表达的非神经性乙酰胆碱的合成和释放。该组织不含胆碱能神经元,即可以排除神经元乙酰胆碱的污染。绒毛的胆碱乙酰转移酶(ChAT)活性为0.65 nmol/mg蛋白质每小时,并含有500 nmol乙酰胆碱/g干重。在不存在胆碱酯酶抑制剂的情况下,从分离的绒毛片中释放的乙酰胆碱为每10分钟1.3 nmol/g湿重,对应于每分钟0.13%的部分释放速率。以下物质没有显著改变乙酰胆碱的释放:氧震颤素(1 µM)、东莨菪碱(1 µM)、(+)-筒箭毒碱(30 µM)、毛喉素(30 µ M)、哇巴因(10 µM)、4α-佛波醇12,13-二癸酸酯(1 µM)和河豚毒素(1 µM)。去除细胞外钙,佛波醇12,13-二丁酸酯(1 μM)和秋水仙碱(100 μM)减少乙酰胆碱释放30%至50%。高浓度氯化钾(54 mM和108 mM)略微增加乙酰胆碱释放(约30%)。浓度为10 µM的尼古丁无效,但100 µM尼古丁在50分钟内逐渐增强乙酰胆碱的释放,而不会使反应脱敏。尼古丁的易化作用被30 µM(+)-筒箭毒碱阻止。胆碱酯酶抑制剂(毒扁豆碱、新斯的明; 3 µM)促进乙酰胆碱外排约6倍,(+)-筒箭毒碱(30 µM)和东莨菪碱(1 µM)联合使用可使增强作用减半。总之,释放机制不同之间的非神经元和神经元乙酰胆碱。存在易化性尼古丁受体,其通过应用尼古丁或通过阻断胆碱酯酶而被激活。因此,胆碱酯酶抑制剂通过两种机制增加测定的乙酰胆碱,保护水解和刺激易化尼古丁受体。
Abstract. The synthesis and release of non-neuronal acetylcholine, a widely expressed signaling molecule, were investigated in the human placenta. This tissue is free of cholinergic neurons, i.e. a contamination of neuronal acetylcholine can be excluded. The villus showed a choline acetyltransferase (ChAT) activity of 0.65 nmol/mg protein per h and contained 500 nmol acetylcholine/g dry weight. In the absence of cholinesterase inhibitors the release of acetylcholine from isolated villus pieces amounted to 1.3 nmol/g wet weight per 10 min corresponding to a fractional release rate of 0.13% per min. The following substances did not significantly modify the release of acetylcholine: oxotremorine (1 µM), scopolamine (1 µM), (+)-tubocurarine (30 µM), forskolin (30 µM), ouabain (10 µM), 4α-phorbol 12,13-didecanoate (1 µM) and tetrodotoxin (1 µM). Removal of extracellular calcium, phorbol 12,13-dibutyrate (1 µM) and colchicine (100 µM) reduced the acetylcholine release between 30% and 50%. High potassium chloride (54 mM and 108 mM) increased the acetylcholine release slightly (by about 30%). A concentration of 10 µM nicotine was ineffective, but 100 µM nicotine enhanced acetylcholine release gradually over a 50-min period without desensitization of the response. The facilitatory effect of nicotine was prevented by 30 µM (+)-tubocurarine. Inhibitors of cholinesterase (physostigmine, neostigmine; 3 µM) facilitated the efflux of acetylcholine about sixfold, and a combination of both (+)-tubocurarine (30 µM) and scopolamine (1 µM) halved the enhancing effect. In conclusion, release mechanisms differ between non-neuronal and neuronal acetylcholine. Facilitatory nicotine receptors are present which are activated by applied nicotine or by blocking cholinesterase. Thus, cholinesterase inhibitors increase assayed acetylcholine by two mechanisms, protection of hydrolysis and stimulation of facilitatory nicotine receptors.
DOI: --
发表时间: 1987
期刊: The Journal of pharmacology and experimental therapeutics
影响因子: --
作者:
Yau,WM;Dorsett,JA;Youther,ML
通讯作者: Youther,ML
佛波酯产生的乙酰胆碱释放的增加不是由运动神经末梢的蛋白激酶 C 介导的。
DOI: --
发表时间: 1998
期刊: The Journal of pharmacology and experimental therapeutics
影响因子: --
作者:
Searl,TJ;Silinsky,EM
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DOI: --
发表时间: 1997
期刊: The Journal of pharmacology and experimental therapeutics.
影响因子: --
作者:
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通讯作者: Owyang,C