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不依赖Ca2+的藜芦碱诱发的纹状体切片乙酰胆碱释放不受囊泡胺转运体抑制剂(AH5183)的抑制:不同递质池的动员。

Ca2+o-independent veratridine-evoked acetylcholine release from striatal slices is not inhibited by vesamicol (AH5183): mobilization of distinct transmitter pools.

作者信息

Adam-Vizi V, Deri Z, Vizi E S, Sershen H, Lajtha A

机构信息

2nd Institute of Biochemistry, Semmelweis University of Medicine, Budapest, Hungary.

出版信息

J Neurochem. 1991 Jan;56(1):52-8. doi: 10.1111/j.1471-4159.1991.tb02561.x.

DOI:10.1111/j.1471-4159.1991.tb02561.x
PMID:1987325
Abstract

The effect of 2-(4-phenylpiperidino)cyclohexanol (AH5183 or vesamicol), a compound known to block the uptake of acetylcholine (ACh) into cholinergic synaptic vesicles, on the release of endogenous and [14C]ACh from slices of rat striatum was investigated. ACh release was evoked either by electrical stimulation or by veratridine. The effect of electrical stimulation was entirely dependent on external Ca2+. By contrast, veratridine (40 microM) also enhanced ACh release in the absence of Ca2+. Indeed, with veratridine two components were clearly distinguished: one dependent on external Ca2+ and the other not. Vesamicol inhibited [14C]ACh release evoked by both veratridine and electrical stimulation in the presence of external Ca2+, provided it was added to the tissue prior to loading with [14C]choline. With the same treatment vesamicol only slightly affected the release of endogenous ACh. Under the same conditions the Ca2(+)-independent [14C]ACh release evoked by veratridine was not prevented by vesamicol. The differential responsiveness to vesamicol suggests that ACh pools involved in Ca2+o-dependent ACh release are different from those mobilized during Ca2+o-independent ACh release.

摘要

研究了2-(4-苯基哌啶基)环己醇(AH5183或维生米可)对大鼠纹状体切片中内源性乙酰胆碱(ACh)和[14C]ACh释放的影响,该化合物已知可阻断ACh摄取到胆碱能突触小泡中。通过电刺激或藜芦碱诱发ACh释放。电刺激的作用完全依赖于细胞外Ca2+。相比之下,藜芦碱(40 microM)在无Ca2+的情况下也能增强ACh释放。实际上,对于藜芦碱,可清楚区分出两个成分:一个依赖于细胞外Ca2+,另一个则不依赖。在存在细胞外Ca2+的情况下,若在向组织中加载[14C]胆碱之前加入维生米可,则它会抑制由藜芦碱和电刺激诱发的[14C]ACh释放。采用相同处理时,维生米可仅轻微影响内源性ACh的释放。在相同条件下,维生米可不能阻止藜芦碱诱发的不依赖Ca2+的[14C]ACh释放。对维生米可的不同反应性表明,参与依赖细胞外Ca2+的ACh释放的ACh池与在不依赖细胞外Ca2+的ACh释放过程中动员的ACh池不同。

相似文献

1
Ca2+o-independent veratridine-evoked acetylcholine release from striatal slices is not inhibited by vesamicol (AH5183): mobilization of distinct transmitter pools.不依赖Ca2+的藜芦碱诱发的纹状体切片乙酰胆碱释放不受囊泡胺转运体抑制剂(AH5183)的抑制:不同递质池的动员。
J Neurochem. 1991 Jan;56(1):52-8. doi: 10.1111/j.1471-4159.1991.tb02561.x.
2
Parameters not influenced by vesamicol: membrane potential, calcium uptake, and internal calcium concentration of synaptosomes.不被维生霉素影响的参数:突触体的膜电位、钙摄取及细胞内钙浓度。
Neurochem Res. 1992 Jun;17(6):539-44. doi: 10.1007/BF00968780.
3
Effect of 2-(4-phenylpiperidino)cyclohexanol on acetylcholine release and subcellular distribution in rat striatal slices.2-(4-苯基哌啶基)环己醇对大鼠纹状体切片中乙酰胆碱释放及亚细胞分布的影响
J Neurochem. 1986 Nov;47(5):1627-33. doi: 10.1111/j.1471-4159.1986.tb00805.x.
4
Acetylcholine mobilization in a sympathetic ganglion in the presence and absence of 2-(4-phenylpiperidino)cyclohexanol (AH5183).在存在和不存在2-(4-苯基哌啶基)环己醇(AH5183)的情况下,交感神经节中乙酰胆碱的动员情况。
J Neurochem. 1988 Jan;50(1):112-21. doi: 10.1111/j.1471-4159.1988.tb13237.x.
5
In favour of the vesicular hypothesis: neurochemical evidence that vesamicol (AH5183) inhibits stimulation-evoked release of acetylcholine from neuromuscular junction.支持囊泡假说的证据:神经化学证据表明,vesamicol(AH5183)可抑制神经肌肉接头处由刺激诱发的乙酰胆碱释放。
Br J Pharmacol. 1989 Nov;98(3):898-902. doi: 10.1111/j.1476-5381.1989.tb14619.x.
6
Mobilization of the readily releasable pool of acetylcholine from a sympathetic ganglion by tityustoxin in the presence of vesamicol.在存在vesamicol的情况下,由tityustoxin从交感神经节动员乙酰胆碱的易释放池。
J Neurochem. 1992 Aug;59(2):544-52. doi: 10.1111/j.1471-4159.1992.tb09404.x.
7
Effect of 2-(4-phenylpiperidino)cyclohexanol (AH 5183) on the veratridine-induced increase in acetylcholine synthesis by rat hippocampal tissue.2-(4-苯基哌啶基)环己醇(AH 5183)对藜芦碱诱导的大鼠海马组织乙酰胆碱合成增加的影响。
J Neurochem. 1988 Sep;51(3):808-19. doi: 10.1111/j.1471-4159.1988.tb01816.x.
8
The effect of the acetylcholine transport blocker 2-(4-phenylpiperidino) cyclohexanol (AH5183) on the subcellular storage and release of acetylcholine in mouse brain.乙酰胆碱转运阻滞剂2-(4-苯基哌啶基)环己醇(AH5183)对小鼠脑内乙酰胆碱亚细胞储存和释放的影响。
Brain Res. 1985 Dec 9;358(1-2):200-9. doi: 10.1016/0006-8993(85)90964-3.
9
Mobilization of a vesamicol-insensitive pool of acetylcholine from a sympathetic ganglion by ouabain.哇巴因对交感神经节中对囊泡乙酰胆碱转运体不敏感的乙酰胆碱池的动员作用。
J Neurochem. 1993 Jul;61(1):45-56. doi: 10.1111/j.1471-4159.1993.tb03536.x.
10
Release of acetylcholine from rat brain synaptosomes by various agents in the absence of external calcium ions.在无细胞外钙离子的情况下,多种试剂对大鼠脑突触体乙酰胆碱释放的影响
J Physiol. 1984 Aug;353:505-21. doi: 10.1113/jphysiol.1984.sp015348.

引用本文的文献

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Exocytotic release of [3H]-acetylcholine by ouabain involves intracellular Ca2+ stores in rat brain cortical slices.哇巴因引起的[3H]-乙酰胆碱胞吐释放涉及大鼠脑皮质切片中的细胞内钙储存。
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Characterization of the carrier-mediated [3H]GABA release from isolated synaptic plasma membrane vesicles.
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Parameters not influenced by vesamicol: membrane potential, calcium uptake, and internal calcium concentration of synaptosomes.不被维生霉素影响的参数:突触体的膜电位、钙摄取及细胞内钙浓度。
Neurochem Res. 1992 Jun;17(6):539-44. doi: 10.1007/BF00968780.