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首页> 外文期刊>The European Journal of Neuroscience >Regulation of acetylcholine release by muscarinic receptors at the mouse neuromuscular junction depends on the activity of acetylcholinesterase.
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Regulation of acetylcholine release by muscarinic receptors at the mouse neuromuscular junction depends on the activity of acetylcholinesterase.

机译：毒蕈碱受体在小鼠神经肌肉接头处对乙酰胆碱释放的调节取决于乙酰胆碱酯酶的活性。

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摘要

Muscarinic acetylcholine receptors (mAChRs) play an important role in regulating the release of acetylcholine (ACh) in various tissues. We used subtype-specific antibodies and a fluorescent-labelled muscarinic toxin to demonstrate that mammalian neuromuscular junction expresses mAChR subtypes M1 to M4, and that localization of all subtypes is highly restricted to the innervated part of the muscle. To elucidate the roles of the mAChR subtypes regulating ACh release, we measured the mean quantal content of endplate potentials in isolated mouse phrenic--hemidiaphragm preparations in which release was reduced by a low Ca2+/high Mg2+ medium. Muscarine decreased evoked ACh release in normal junctions but, depending on the concentration, reduced or increased transmitter release in collagen Q-deficient junctions completely lacking acetylcholinesterase (AChE). Both effects were also seen in normal junctions when AChE was inhibited by various doses of fasciculin-2. Block of mAChRs by atropine had no effect on evoked release at normal junctions, but decreased release at junctions lacking AChE. The muscarine-elicited depression of ACh release in normal junctions was completely abolished by pertussis toxin or methoctramine pretreatment, but was not affected by muscarinic toxin MT-3, thus indicating the involvement of the M2 mAChR. The muscarine-induced increase of ACh release in AChE-deficient junctions was not affected by pertussis toxin, but was completely blocked by MT-7, a specific M1 mAChR antagonist. Our results show that the M1 and M2 mAChRs have opposite presynaptic functions in modulating quantal ACh release, and that regulation of release by the two receptor subtypes depends on the functional state of AChE at the neuromuscular junction.
机译：毒蕈碱型乙酰胆碱受体（mAChRs）在调节各种组织中乙酰胆碱（ACh）的释放中起重要作用。我们使用亚型特异性抗体和荧光标记的毒蕈碱毒素来证明哺乳动物神经肌肉接头表达mAChR亚型M1至M4，并且所有亚型的定位都高度限于肌肉的神经支配部分。为了阐明mAChR亚型调节ACh释放的作用，我们测量了分离的小鼠-半ph制品中终板电位的平均定量含量，其中低Ca2 + /高Mg2 +培养基可降低释放。毒蕈碱可降低正常接头中诱发的ACh释放，但取决于浓度，完全缺乏乙酰胆碱酯酶（AChE）的胶原Q缺陷接头中的递质释放减少或增加。当不同剂量的fasciculin-2抑制AChE时，在正常的连接处也可以看到这两种作用。阿托品对mAChRs的阻滞对正常交界处的诱发释放没有影响，但在缺乏AChE的交界处释放降低。毒蕈碱引起的正常连接处ACh释放的抑制已被百日咳毒素或甲氧苄明预处理完全消除，但不受毒蕈碱毒素MT-3的影响，因此表明M2 mAChR参与其中。毒蕈碱诱导的AChE缺陷连接中ACh释放增加不受百日咳毒素的影响，但被MT-7（一种特定的M1 mAChR拮抗剂）完全阻断。我们的结果表明，M1和M2 mAChRs在调节定量ACh释放中具有相反的突触前功能，并且两种受体亚型对释放的调节取决于神经肌肉接头处AChE的功能状态。

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