Inotropism and Contracture of Aplysiid Ventricles as Related to the Action of Neurohumors on Resting and Action Potentials of Molluscan Hearts
Inotropism and Contracture of Aplysiid Ventricles as Related to the Action of Neurohumors on Resting and Action Potentials of Molluscan Hearts
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海兔心室的正性肌力和挛缩与神经体液对软体动物心脏静息和动作电位的作用有关
DOI：
10.1093/icb/19.1.145
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发表时间：
1979
影响因子：
2.6
通讯作者：
R. Yantorno
中科院分区：
文献类型：
--
作者：
R. Hill;R. Yantorno
神经体液对软体动物肌肉的突触后作用既有兴奋和抑制作用，也有力的控制作用。力的控制可能表现为对兴奋反应的增强，自发收缩中的变力性增强，或紧张性的增加。我们已经把注意力集中在应用假定的神经体液引起的无脑心室力的改变上。结果被解释在已知的神经体液对软体动物心脏的静息电位和动作电位的影响。我们用一个蔗糖间隙装置和一个力-位移传感器在细胞外记录了豚鼠心室的复合膜电位，以测量收缩或挛缩时的力。加州无尾两栖动物心室的膜电位为−52.5 ± 9.4 mV。增加外部钾离子浓度，会使指状裸腹蛛或加州裸腹蛛的囊泡去极化，并伴有挛缩。在无钙培养基中孵育后，KCl收缩力直接依赖于钙离子浓度。在无钾介质中，8.3 ±2.14 mV的去极化被锂替代介质中的钠所阻断，这表明了产电钠泵。在低氯介质中存在持续的去极化，这表明氯对静息电位有显著的贡献。Dolabella auriculana或Aaplasia dactylomela的神经节被乙酰胆碱（ACh）去极化。除极阈值低于收缩力阈值。A. 5-羟色胺（5-HT）使Dactylomela去极化，阈值为10−9 M，最大去极化为30 mV（10− 4 M）。5-HT去极化可引起搏动，但不引起挛缩。Ach抑制心室搏动，但Ach不使Ach去极化，低浓度Ach可使强直性挛缩的去极化心室超极化和舒张。Dolabella auricularia心室的收缩力取决于心脏动作电位平台期的持续时间。5 HT使平台期延长，伴随着搏动力的增加，ACh使平台期缩短，伴随着搏动力的减少。结果表明，加州滨藜心室肌动作电位不分峰期和平台期，ACh和5-HT对动作电位的形态无明显影响。然而，耳形多拉贝拉、南极虾和加州虾的心室都能被5-羟色胺兴奋，其阈值约为10−M。A.加州心室因缺乏钠离子而被5 HT阻断，这可能是软体动物心脏起搏器电位的原因。
The postsynaptic actions of neurohumors on molluscan muscle may be exerted through control of force as well as by means of excitation and inhibition. The control of force may appear as potentiation of the response to excitation, as increased inotropism in spontaneous contractions, or as an increase in tonus. We have directed our attention to the alterations of force induced in aplysiid ventricles by applied postulated neurohumors. The results are interpreted in terms of the known effects of neurohumors on resting potential and action potentials of molluscan hearts. We recorded compound membrane potentials of aplysiid ventricles extracellularly, using a single sucrose gap apparatus together with a force-displacement transducer to measureforce in contractions or contracture. Aplysia californica ventricle has a membrane potential of −52.5 ± 9.4 mV. Ventricles of Aplysia dactylomela or Aplysia californica are depolarized by increased concentrations of external potassium ion, with an accompanying contracture. After incubation in calcium-free medium, KCl contracture-force is directly dependent on calcium ion concentration. A depolarization of 8.3 ±2.14 mV in potassium-free medium is blocked by substitution of lithium for sodium in the medium, suggesting an electrogenic sodium pump. There is a sustained depolarization in low chloride medium, which suggests a significant chloride contribution to the resting potential. Ventricles of Dolabella auriculana or Aplysia dactylomela are depolarized by acetylcholine (ACh). Threshold for depolarization is lower than threshold for contracture-force. The ventricle of A. dactylomela is depolarized by 5- hydroxytryptamine (5HT) with threshold at 10−9 M and a maximum depolarization of 30 mV at 10−4M. Depolarization by 5HT may induce beating but does not induce contracture. Ventricles of Aplysia californica are not depolarized by ACh although beating ventricles are inhibited, and a depolarized ventricle in a tonic contracture may be hyperpolarized and relaxed by low concentrations. The force of contraction of the ventricle of Dolabella auricularia is dependent on the duration of the plateau phase of the cardiac action potential. The plateau is lengthened by 5HT with an accompanying increase in force of beat, and shortened by ACh, with an accompanying decrease in force of beat. The action potential in the ventricle of Aplysia californica is not differentiated into spike and plateau phases, and neither ACh nor 5HT has any marked effect on the form of the action potential. Nevertheless, isolated ventricles of Dolabella auricularia , Aplysia dactylomela , and Aplysia californica are all excited by 5-hydroxytryptamine, with a threshold at about 10−M. Both spontaneous beating and excitation induced in A. californica ventricles by 5HT are blocked by lack of the sodium ion, which may be responsible for pacemaker potentials in molluscan hearts.