首页> 外文期刊>Toxicon: An International Journal Devoted to the Exchange of Knowledge on the Poisons Derived from Animals, Plants and Microorganisms >Effects of trachynilysin, a protein isolated from stonefish (Synanceia trachynis) venom, on frog atrial heart muscle
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Effects of trachynilysin, a protein isolated from stonefish (Synanceia trachynis) venom, on frog atrial heart muscle

机译:从石头鱼(Synanceia trachynis)毒液中分离出的一种蛋白质曲曲霉素对蛙心房肌的影响

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The effects of trachynilysin (TLY), a protein toxin isolated from stonefish (Synanceia trachynis) venom, were studied on the electrical and mechanical activities of frog atrial fibres. TLY (1 mu g/ml) hyperpolarized the membrane, shortened the action potential (AP) duration (APD), exerted a negative inotropic effect and elicited contracture. These effects did not develop in the presence of atropine. TLY shortened the APD of fibres isolated from a frog completely paralyzed with botulinum type A toxin, in the presence of Ca2+ but not when Ca2+ was replaced by Sr2+. TLY increased the basal and the peak of the fluorescence ratio of stimulated fibres loaded with fura-2. Confocal laser scanning microscopy revealed the existence of a diffuse innervation in atrial tissue. Our results suggest that TLY enhances the release of acetylcholine from atrial cholinergic nerve terminals and activates indirectly muscarinic receptors leading to a shortening of APD. They also show that the mechanical effects induced by TLY are due to an increase of the Ca2+ influx and to a rise in intracellular Ca2+ levels which leads to (i) a slowing of the Na+/Ca2+ exchange activity, which accounts for the contracture and (ii) the activation of a Ca2+-dependent K+ current involved in the ADP shortening. (C) 2000 Elsevier Science Ltd. All rights reserved. [References: 33]
机译:研究了从石头鱼(Synanceia trachynis)毒液中分离出的一种蛋白质毒素-曲奇溶素(TLY)对蛙心房纤维的电和机械活性的影响。 TLY(1μg / ml)使膜超极化,缩短动作电位(AP)持续时间(APD),发挥负性肌力作用并引起挛缩。在存在阿托品的情况下不会产生这些作用。在存在Ca2 +的情况下,TLY缩短了从完全被A型肉毒杆菌麻痹的青蛙中分离出的纤维的APD含量,但是当Ca2 +被Sr2 +替代时却没有。 TLY增加了装有fura-2的受激纤维的荧光比率的基数和峰值。共聚焦激光扫描显微镜揭示了在心房组织中存在弥漫性神经支配。我们的结果表明,TLY增强了乙酰胆碱从心房胆碱能神经末梢的释放,并间接激活了毒蕈碱受体,从而导致APD缩短。他们还表明,TLY诱导的机械作用是由于Ca2 +流入量增加和细胞内Ca2 +水平升高导致的,这导致(i)Na + / Ca2 +交换活性减慢,这是挛缩和( ii)激活涉及ADP缩短的Ca2 +依赖性K +电流。 (C)2000 Elsevier ScienceLtd。保留所有权利。 [参考:33]

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