Abstract

Using electrophysiology, the effect of nicotinic acetylcholine receptor (nAChR) ligands on acetylcholine-induced depolarization in the neurons of Helix lucorum snail was studied. It was found that the α-conotoxin PnIA [R9, L10], a selective antagonist of α7 nAChR, and α-cobratoxin (antagonist of α7 and muscle-type nAChR) suppressed neuronal depolarization. Fluorescence microscopy showed staining of the neurons with fluorescently labeled α-bungarotoxin; this staining was reduced by pretreatment with α-cobratoxin. Induced depolarization was also suppressed by α-conotoxin RgIA, a selective inhibitor of α9 nAChR. In contrast to Lymnaea stagnalis nAChR, which are weakly sensitive to neurotoxin II and α-conotoxin GI, antagonists of muscle-type nAChR, H. lucorum receptors were most effectively inhibited by these antagonists. The results obtained, as well as the previously found sensitivity of the receptors studied in this work to muscarinic receptor ligands, indicate an unusual atypical pharmacological profile of H. lucorum nAChR.

中文翻译：

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土耳其蜗牛神经元上的非典型乙酰胆碱受体。

摘要

使用电生理学，研究了烟碱乙酰胆碱受体（nAChR）配体对lu螺神经元中乙酰胆碱诱导的去极化的影响。发现α-芋螺毒素PnIA [R9，L10]，α7nAChR的选择性拮抗剂，和α-眼镜蛇毒素（α7拮抗剂和肌肉型nAChR）抑制神经元去极化。荧光显微镜显示神经元被荧光标记的α-真菌毒素染色。通过用α-眼镜蛇毒素预处理可以减少这种染色。α-芋螺毒素RgIA（α9nAChR的选择性抑制剂）也抑制了诱导的去极化。与对神经毒素II和α-芋螺毒素GI较不敏感的剑兰nAChR相对，它是肌肉型nAChR，H。lucorum的拮抗剂这些拮抗剂最有效地抑制了受体。所获得的结果，以及先前在这项工作中研究的受体对毒蕈碱受体配体的敏感性，都表明了嗜油杆菌nAChR具有非同寻常的非典型药理特性。