Price David N, Berry Michael S
School of the Environment and Society, Swansea University, Singleton Park, Swansea, SA2 8PP, Wales, UK.
J Chem Ecol. 2008 Aug;34(8):994-1004. doi: 10.1007/s10886-008-9511-6. Epub 2008 Jul 4.
The essential oil constituents citral, geraniol, and eugenol have toxic or repellent properties that are utilized by a variety of organisms to deter natural enemies. Their mechanism of action is unknown, but some essential oils such as eugenol are claimed to act on insects by specific binding to octopamine receptors. We studied their effects on the isolated buccal ganglia of Planorbis corneus, having demonstrated that they caused cessation of feeding and death when added to the aquarium water (approximately 5 x 10(-4) mol l(-1)). They abolished spike activity at 2 x 10(-3) mol l(-1) but at lower doses (threshold 5 x 10(-5) mol l(-1)) they resembled octopamine in eliciting burst firing indicative of the fictive feeding sequence. However, the octopamine antagonists phentolamine (10(-5) mol l(-1)), yohimbine (10(-4) mol l(-1); which blocked hyperpolarizing octopamine responses), and metoclopramide (10(-4) mol l(-1); which blocked depolarization) had no effect on any of the responses to the oils. The oils produced incomplete block of excitatory and inhibitory responses to octopamine even at high doses (10(-3) mol l(-1)), and they had similar effects on responses to dopamine and acetylcholine. The oils (10(-5)-2 x 10(-3) mol l(-1)) all increased the frequency of contractions of the isolated esophagus and progressively reduced their amplitude. The effects were similar to those of octopamine but were not blocked by phentolamine, metoclopramide, or prolonged exposure of the esophagus to octopamine. The results suggest a variety of actions that could contribute to toxic effects in molluscs, but there was no evidence for specific actions on octopamine receptors, either as agonists or antagonists. Evidence is presented that nonspecific depolarization produces their octopamine-like actions.
香茅醛、香叶醇和丁香酚等精油成分具有毒性或驱避特性,多种生物利用这些特性来抵御天敌。它们的作用机制尚不清楚,但一些精油如丁香酚据称通过与章鱼胺受体特异性结合来作用于昆虫。我们研究了它们对角扁卷螺离体颊神经节的影响,已证明将它们添加到水族箱水中(约5×10⁻⁴摩尔/升)会导致摄食停止和死亡。它们在2×10⁻³摩尔/升时消除了动作电位活动,但在较低剂量(阈值5×10⁻⁵摩尔/升)时,它们类似于章鱼胺,引发指示虚构摄食序列的爆发式放电。然而,章鱼胺拮抗剂酚妥拉明(10⁻⁵摩尔/升)、育亨宾(10⁻⁴摩尔/升;阻断章鱼胺的超极化反应)和甲氧氯普胺(10⁻⁴摩尔/升;阻断去极化)对精油的任何反应均无影响。即使在高剂量(10⁻³摩尔/升)下,这些精油对章鱼胺的兴奋性和抑制性反应也只能产生不完全阻断,并且它们对多巴胺和乙酰胆碱的反应也有类似影响。这些精油(10⁻⁵ - 2×10⁻³摩尔/升)均增加了离体食管的收缩频率,并逐渐降低其幅度。这些作用与章鱼胺相似,但不受酚妥拉明、甲氧氯普胺或食管长时间暴露于章鱼胺的阻断。结果表明存在多种可能导致对软体动物产生毒性作用的作用方式,但没有证据表明其对章鱼胺受体有特异性作用,无论是作为激动剂还是拮抗剂。有证据表明非特异性去极化产生了它们类似章鱼胺的作用。