Modulation of crayfish superficial extensor muscles by a FMRFamide-related neuropeptide

Patricia A. Quigley , A.Joffre Mercier
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引用次数: 18

Abstract

The superficial extensor muscles of the crayfish abdomen were examined as a possible site for modulation by DF2 (Asp-Arg-Asn-Phe-Leu-Arg-Phe-NH2), a FMRFamide-related neuropeptide found in crayfish pericardial organs (26). The superficial extensor muscles are of the tonic type and generate slow contractions that affect posture. DF2, at concentrations of 10−8 M or higher, increased muscle tonus in isolated, unstimulated neuromuscular preparations. In some preparations, the peptide also induced small, arrhythmic contractions or increased the amplitude of such contractions if they were already present. The spontaneous contractions were temperature-dependent and insensitive to 10−7 M tetrodotoxin, indicating that they were myogenic. DF2 increased muscle tonus in the presence of tetrodotoxin and when nerve-evoked contractions were blocked using Joro spider toxin (JSTX), a glutamate receptor antagonist. Thus, the effects of DF2 on contraction appear to represent direct effects on the muscle and not changes in release of chemical transmitter from nerve terminals. DF2 did not alter resting membrane potential or input resistance in the muscle fibres.

The effects of DF2 on contraction were blocked by the Ca2+ channel antagonists Mn2+ Ni2+ and Cd2+ and nicardipine, and by replacing extracellular Ca2+ with Mg2+. This suggests that the peptide's effect may require an influx of extracellular Ca2+ through dihydropyridine-sensitive Ca2+ channels. The Ca2+ channel antagonists also reduced muscle tonus on their own, suggesting that they may lower the intracellular calcium concentration. The peptide might act by enhancing Ca2+ influx or by enhancing Ca2+-dependent release of Ca2+ ions from internal stores.

fmrfamily相关神经肽对小龙虾浅表伸肌的调节作用
我们研究了小龙虾腹部的浅表伸肌作为DF2 (asp - arg - asn - ph - leu - arg - ph - nh2)可能调控的部位,DF2是一种存在于小龙虾心包器官中的fmrfamily相关神经肽(26)。浅表伸肌属于强直型,产生影响姿势的缓慢收缩。DF2浓度为10 - 8 M或更高时,可使分离的、未受刺激的神经肌肉制剂中的肌肉张力增加。在某些制剂中,该肽还会引起小的、心律失常的收缩,或者如果收缩已经存在,则会增加这种收缩的幅度。自发收缩是温度依赖性的,对10 - 7 M河豚毒素不敏感,表明它们是肌源性的。当使用谷氨酸受体拮抗剂Joro蜘蛛毒素(JSTX)阻断神经诱发的收缩时,DF2增加了河豚毒素存在的肌肉张力。因此,DF2对收缩的影响似乎代表了对肌肉的直接影响,而不是神经末梢释放化学递质的变化。DF2不改变肌纤维的静息膜电位或输入电阻。DF2对收缩的影响被Ca2+通道拮抗剂Mn2+ Ni2+和Cd2+和尼卡地平阻断,并被Mg2+取代细胞外Ca2+。这表明肽的作用可能需要通过二氢吡啶敏感的Ca2+通道流入细胞外Ca2+。Ca2+通道拮抗剂本身也能减少肌肉张力,这表明它们可能降低细胞内钙浓度。该肽可能通过增强Ca2+内流或通过增强Ca2+依赖的Ca2+离子从内部储存的释放而起作用。
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