Neuropharmacological studies of Schistosoma mansoni were conducted in vitro using visual observations of motor activity and measurements of worm length and extracellular electrical activity. The instrumentation and methodology described quantitatively measure extracellular electrical potentials associated with motor activity, and provide a highly sensitive, objective technique for studying effects of antischistosomal compounds and for evaluating schistosomes as a model for neuropharmacological investigation. The visual motor and electrical responses of schistosomes to various pharmacological agents support earlier claims for the presence of an excitatory tryptaminergic system and an inhibitory cholinergic system. The stimulation of motor activity by 5-hydroxytryptamine was blocked by the antagonists metergoline and cyproheptadine in a dose-dependent manner. The hypermotility induced by cholinergic blockade (atropine or mecamylamine) or 5-hydroxytryptamine release (p-chlorophenylethylamine) was abolished by these antagonists. The cholinomimetic agents, acetylcholine, carbachol and arecoline, and the cholinesterase inhibitors neostigmine and metrifonate, caused a flaccid paralysis of schistosomes. Carbachol-induced paralysis was reversed by both the nicotinic cholinergic blocker, mecamylamine, and the muscarinic cholinergic blocker, atropine. This reversal occurred in a dose-dependent manner. It is suggested that the cholinoceptive site in S. mansoni has unique pharmacological properties, distinctly different from those in mammals. Dopamine, apomorphine, epinephrine and norepinephrine had little effect on schistosome motility, but produced marked increases in worm length. The dopaminergic antagonist, haloperidol, completely blocked the dopamine response. A broad range of putative amino acid neurotransmitters failed to alter schistosome motor activity. The simple nervous system of the schistosome appears to have many unique pharmacological features which may make it a useful model for the study of drugs for human use, as well as providing an effective point for chemotherapeutic attack.

译文

:曼氏血吸虫的神经药理研究是在体外进行的,采用运动活动的目测观察和蠕虫长度及细胞外电活动的测量。描述的仪器和方法定量地测量了与运动活动相关的细胞外电位,并为研究抗血吸虫病化合物的作用和评估血吸虫病作为神经药理学研究的模型提供了一种高度灵敏,客观的技术。血吸虫对各种药理剂的视觉运动和电反应支持了较早的关于存在兴奋性色胺能系统和抑制性胆碱能系统的主张。 5-羟色胺对运动活性的刺激被拮抗剂美特古林和赛庚啶阻断,呈剂量依赖性。这些拮抗剂消除了胆碱能阻滞(阿托品或美加明)或5-羟色胺释放(对氯苯基乙胺)引起的运动过快。拟胆碱药,乙酰胆碱,卡巴胆碱和槟榔碱,以及胆碱酯酶抑制剂新斯的明和美甲芬酯,导致血吸虫的松弛性麻痹。烟碱型胆碱能阻滞剂美卡明胺和毒蕈碱型胆碱能阻滞剂阿托品逆转了卡巴胆碱引起的瘫痪。这种逆转以剂量依赖性方式发生。有人提出曼氏葡萄球菌的胆汁感受性位点具有独特的药理特性,与哺乳动物的明显不同。多巴胺,阿扑吗啡,肾上腺素和去甲肾上腺素对血吸虫的蠕动影响不大,但蠕虫长度却明显增加。多巴胺能拮抗剂氟哌啶醇完全阻断了多巴胺反应。广泛的推定氨基酸神经递质未能改变血吸虫的运动活性。血吸虫的简单神经系统似乎具有许多独特的药理特性,这可能使其成为研究人类使用药物的有用模型,并为化学疗法的发作提供有效的方法。

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