副交感神经节细胞5─羟色胺去极化反应的离子基础

使用离体细胞内记录，研究了猫副交感性胰腺神经节细胞的５－羟色胺（５－ＨＴ）去极化反应及其离子基础。５－ＨＴ使大部份细胞（４７／５１）产生去极化反应。反应只有两种类型：快去极化（６／４７）及慢去极化（３５／４７），另有６个细胞出现先快、后慢的双相去极化反应；５－ＨＴ导致的快去极化伴有膜电阻减小，向细胞内通以超极化直流电形成条件性膜超极时其幅度增大，提示Ｎａ＋导增大是其离子基础；５－ＨＴ导致的不同细胞的慢去极化分别伴随膜电阻增大、减小或不变，条件性膜超极时其幅度分别增大或不变，提示不是单一离子、而是多种离子参与其形成。分别用低Ｎａ＋、高Ｋ＋溶液灌注神经节，５－ＨＴ慢去极化均明显减小，而低Ｃｌ－溶液则无明显效应，表明Ｎａ＋导增大和／或Ｋ＋导减少是５－ＨＴ慢去极化的离子基础。     

离子敏感微电极的制作及参数测试

本文制作了Ｋ＋，Ｎａ＋液态膜离子敏感微电极（Ｋ＋，Ｎａ＋—ＩＳＭＥ），并稳定了其制作条件，经测试，Ｋ＋—ＩＳＭＥ线性范围为１—１０－４ｍｏｌ／Ｌ，检测下限为３．０×１０－６ｍｏｌ／Ｌ。对Ｎａ＋选择系数为２．６８×１０－４。电位飘移为±０．１ｍＶ／ｈ。Ｎａ＋—ＩＳＭＥ线性范围为１—２．０×１０－ｍｏｌ／Ｌ，检测下限为５．０×１．０－４ｍｏｌ／Ｌ。对Ｋ＋的选择系数为１．８５×１０－２，对Ｃａ２＋的选择系数为１．４６。上述参数均满足生理实验要求，离子敏感微电极技术可做为生理学研究的重要手段。     

苏云金杆菌δ—内毒素对离体昆虫细胞作用机制的研究

利用ＢａｃｉｌｌｕｓｔｈｕｒｉｎｇｉｅｎｉｓｉｓＨＤ－１δ－内毒素作用离体培养的昆虫细胞（Ｐｘ），并测定其对Ｐｘ细胞葡萄糖Ｎａ＋Ｋ＾＋离子吸收的影响，实验表明，δ－内毒素作用Ｐｘ细胞后０．５ｍｉｎ内细胞对葡萄糖的吸收大量增加，１０ｍｉｎ后，葡萄糖的吸收基本停止，细胞内Ｎａ＾＋含量的快速增加发生在δ－内毒素作用５ｍｉｎ后，Ｋ＾＋离子的含量在１ｍｉｎ后开始增加，但增加缓慢。     

阳离子对猪心细胞色素C的反胶团萃取的影响

在猪心提取液中添加阳离子的情况下，观察了ＡＯＴ／异辛烷反胶团对蛋白质和细胞色素Ｃ的萃取效果。结果表明：萃取分相以添加Ｍｇ（２＋）最好，其次分别为Ｎａ＋．Ｋ＋、Ｃａ（２＋）。在添加Ｍｇ（２＋）、Ｎａ＋，Ｃａ（２＋），Ｋ＋离子后，对蛋白质的萃取率分别为：５０．４％、３１．５％、２９．２％、２７．８％。在添加Ｍｇ（２＋），Ｎａ＋Ｋ＋离子时，对细胞色素的萃取率（以反萃取率表示）分别为４０．６％、３７．４％、＋３０．４％。     

Na_(2.5)Hf_(2-x)Ti_xSi_(1.5)P_(1.5)O_(12)系统快离子导体的阻抗谱

系统地研究了Ｎａ２．５Ｈｆ２－ｘＴｉｘＳｉ１．５Ｐ１．５Ｏ１２快离子导体的阻抗谱，采用ＺＲＥＳ３．３程序对实测点进行解释和拟合计算，结果表明该系统呈良好的低温导电性。其中起始组成为Ｎａ２．５Ｈｆ１．８Ｔｉ０．２Ｓｉ１．５Ｏ１２的电导性最好．在４７３Ｋ时，其导电率σ４７３＝１．４７×１０－２（Ω·ｃｍ）－１，电导激活能Ｅａ＝ ２３．８６ｋＪ／ｍｏｌ．     

钾铵离子选择电极的研制及其在土壤肥料分析中的应用

以亚戊基双（４＇－苯并１５－冠－５）为中性载体，制得对Ｋ￣＋、具有相近响应的ＰＶＣ膜离子选择性电极。Ｎｅｒｎｓｔ线性响应范围１×１０￣（－１）～８×１０￣（－５）ｍｏｌ／Ｌ；响应斜率为５３ｍＶ／ＰＭ；对Ｌｉ￣＋、Ｎａ￣＋、Ｃａ￣（２＋）、Ｍｇ￣（２＋）、Ｂａ￣（２＋）的选择性系数分别为６×１０￣（－５），５×１０￣（－３），３×１０￣（－４），４×１０￣（－４），８×１０￣（－４）。用本电极可快速测出土壤肥料中速效氮、钾的含量。     

川芎嗪对刺激─分泌偶联模型功能活动的抑制作用

用胶原酶消化分离小牛肾上腺髓质嗜铬细胞,１０－４ｍｏｌ／Ｌ乙酰胆碱（Ａｃｈ）促进细胞儿茶酚胺的分泌,其作用具有Ｃａ２＋依赖性,回归方程ｒ＝－３．２９０＋５．２７５ｘ,相关系数Ｒ＝０．９９１０＞＞α０．０１＝０．７９８０．高Ｋ＋（６５ｍｍｏｌ／Ｌ）使膜去极化,也促进细胞儿茶酚胺的分泌,在一定范围内与Ｃａ２＋浓度呈正相关,回归方程ｙ＝１．３７６＋５．３３７ｘ,相关系数Ｒ＝０．９８５６＞＞α０．０１＝０．７９８１．磷酸川芎嗪（ＴＭＰ）浓度为１０－４～１０－７ｍｏｌ／Ｌ时,能抑制Ａｃｈ促进的分泌作用,１０－３～１０－７ｍｏｌ／Ｌ时能抑制高Ｋ＋促进的分泌作用．     

Depolarization Induced by Substance P on Rat Stellate Ganglion Neurons

应用细胞内生物电记录技术，观察神经肽Ｐ物质（ＳＰ）对大鼠星状神经节细胞的影响。ＳＰ在１μｍｏｌ～１０μｍｏｌ或更高的浓度范围内，供试３５个细胞，有２８个细胞发生膜除极反应。用低钙（０．２５ｍｍ）或用含河豚毒素（ＴＴＸ，１μｍｏｌ）克氏液灌流神经节，不影响ＳＰ引起的除极反应的幅度和时程。ＳＰ引起除极反应的同时常伴有膜电阻增大。当膜电位增大时，除极化反应幅度变小，反转电位为－８０ｍＶ至－１００ｍＶ。研究表明，ＳＰ对部分星状神经节细胞具有兴奋作用，使通过这些细胞的信息传递增强；ＳＰ对细胞膜的除极作用是由于其引起细胞膜钾导降低所致。     

高岭石和NaZr_2P_3O_（12）为基的矿物快离子导体

利用天然矿物高岭石为原料，采用高温固相应制备了Ｎａ１＋２ｘＡｌｘＺｒ２－ｘＳｉｘＰ３－ｘＯ１２系统的矿物快离子导体材料．Ｘ射线衍射表明，该材料具有Ｎａｓｉｃｏｎ型的骨架结构，２９８～６７３Ｋ离子电导率为００１～１ｍＳ／ｃｍ，激活能４０５３～５２１１ｋＪ／ｍｏｌ，当ｘ＝０５时呈现最高电导率，在６７３Ｋ时其电导率达到２５ｍＳ／ｃｍ，它的活化能为４０５３ｋＪ／ｍｏｌ     

锑在弱碱溶液中阳极成膜规律的研究

利用恒电位阳极极化电流与极化时间的关系、线性电位扫描及Ｘ射线衍射研究了锑在２．５×１０－５ｍｏｌ／ｍ３ＮａＨＣＯ３＋２．５×１０－５ｍｏｌ／ｍ３Ｎａ２ＣＯ３＋５．０×１０－４ｍｏｌ／ｍ３Ｎａ２ＳＯ４溶液中（ｐＨ＝９．１，３０℃）于１．２Ｖ（ＶＳ．ＳＣＥ）阳极成膜３ｈ，阳极成膜规律及膜相组成与结构。实验结果表明，本工作中的阳极膜主要由Ｓｂ２Ｏ３（斜方）晶体构成，成膜规律为锑的溶解与锑氧离子ＳｂＯ＋的生成→锑氧化物膜的形成与增厚→氧化物膜的钝化。     

P物质对大鼠星状神经节细胞的除极化

应用细胞内生物电记录技术,观察神经肽P物质(SP)对大鼠星状神经节细胞的影响.SP在1 μmol～10 μmol或更高的浓度范围内,供试35个细胞, 有28个细胞发生膜除极反应.用低钙(0.25 mm)或用含河豚毒素(TTX,1 μmol)克氏液灌流神经节,不影响SP引起的除极反应的幅度和时程.SP引起除极反应的同时常伴有膜电阻增大.当膜电位增大时,除极化反应幅度变小,反转电位为-80 mV至-100 mV.研究表明,SP对部分星状神经节细胞具有兴奋作用,使通过这些细胞的信息传递增强;SP对细胞膜的除极作用是由于其引起细胞膜钾导降低所致.     

P物质对大鼠星状神经节细胞的影响

应用细胞内生物电记录方法，观察神经肽Ｐ物质（ＳＰ）对大鼠星状神经节能细胞的影响，用灌流或用加压向细胞周围施加ＳＰ可使部分细胞发生膜除极反应，用低钙或用含河豚毒素克氏液灌流神经节，并不影响ＳＰ引起的除极反应的幅度和时程。ＳＰ引起除极反应的同时常伴有膜电阻增大，当膜电位增大时，除极化反应幅度变小，反转电位为－８０ｍＶ至－１００ｍＶ，研究表明，ＳＰ对部分星状神经节细胞具有直接兴奋作用，并且ＳＰ对细胞膜的     

Subthreshold Na+-dependent theta-like rhythmicity in stellate cells of entorhinal cortex layer II

The oscillation of membrane potential in mammalian central neurons is of interest because it relates to the role of oscillations in brain function. It has been proposed that the entorhinal cortex (EC), particularly the stellate cells of layer II (ECIIscs), plays an important part in the genesis of the theta rhythm. These neurons occupy a key position in the neocortex-hippocampus-neocortex circuit, a crucial crossroad in memory functions. Neuronal oscillations typically rely on the activation of voltage-dependent Ca2+ conductances and the Ca2+ -dependent K+ conductance that usually follows, as seen in other limbic subcortical structures generating theta rhythmicity. Here we report, however, that similar oscillations are generated in ECIIscs by a Na+ conductance. The finding of a subthreshold, voltage-gated, Na+ -dependent rhythmic membrane oscillation in mammalian neurons indicates that rhythmicity in heterogeneous neuronal networks may be supported by different sets of intrinsic ionic mechanisms in each of the neuronal elements involved.     

Beta-adrenoceptor agonists increase membrane K+ conductance in cardiac Purkinje fibres

Hormonal modulation of the ionic conductance of cell membranes is a topic of considerable current interest; it has a major role, for example, in the improved performance of the vertebrate heart elicited by sympathetic nerve stimulation or by circulating catecholamines, an effect involving enhanced calcium influx. beta-Agonist catecholamines also abbreviate the action potential of cardiac Purkinje fibres, and increase the resting potential in a variety of cells, including cardiac cells, a hyperpolarization usually attributed to stimulation of the electrogenic Na+/K+ pump. We show here that nanomolar concentrations of beta-catecholamines cause hyperpolarization of cardiac Purkinje fibres, not by increasing Na+/K+ pump current, but by increasing resting membrane K+ conductance. The hyperpolarization and shortening of the action potential should increase availability of Na+ channels and reduce the refractory period, effects tending to safeguard impulse propagation through the ventricular conducting system despite the increased heart rate caused by beta-catecholamine action on the sinus node pacemaker.     

Putative receptor for the cytoplasmic inactivation gate in the Shaker K+ channel

Inactivation of ion channels is important in the control of membrane excitability. For example, delayed-rectifier K+ channels, which regulate action potential repolarization, are inactivated only slowly, whereas A-type K+ channels, which affect action potential duration and firing frequency, have both fast and slow inactivation. Fast inactivation of Na+ and K+ channels may result from the blocking of the permeation pathway by a positively charged cytoplasmic gate such as the one encoded by the first 20 amino acids of the Shaker B (ShB) K+ channel. We report here that mutation of five highly conserved residues between the proposed membrane-spanning segments S4 and S5 (also termed H4) of ShB affects the stability of the inactivated state and alters channel conductance. One such mutation stabilizes the inactivated state of ShB as well as the inactivated state induced in the delayed-rectifier type K+ channel drk1 by the cytoplasmic application of the ShB N-terminal peptide. The S4-S5 loop, therefore, probably forms part of a receptor for the inactivation gate and lies near the channel's permeation pathway.     

Voltage and Ca2+-activated K+ channel in baso-lateral acinar cell membranes of mammalian salivary glands

Nervous or hormonal stimulation of many exocrine glands evokes release of cellular K+ (ref. 1), as originally demonstrated in mammalian salivary glands2,3, and is associated with a marked increase in membrane conductance1,4,5. We now demonstrate directly, by using the patch-clamp technique6, the existence of a K+ channel with a large conductance localized in the baso-lateral plasma membranes of mouse and rat salivary gland acinar cells. The K+ channel has a conductance of approximately 250 pS in the presence of high K+ solutions on both sides of the membrane. Although mammalian exocrine glands are believed not to possess voltage-activated channels1,7, the probability of opening the salivary gland K+ channel was increased by membrane depolarization. The frequency of channel opening, particularly at higher membrane potentials, was increased markedly by elevating the internal ionized Ca2+ concentration, as previously shown for high-conductance K+ channels from cells of neural origin8-10. The Ca2+ and voltage-activated K+ channel explains the marked cellular K+ release that is characteristically observed when salivary glands are stimulated to secrete.     

Inhibition by dopamine of (Na(+)+K+)ATPase activity in neostriatal neurons through D1 and D2 dopamine receptor synergism

The (Na(+)+K+)ATPase, an integral membrane protein located in virtually all animal cells, couples the hydrolysis of ATP to the countertransport of Na+ and K+ ions across the plasma membrane. In neurons, a large portion of cellular energy is expended by this enzyme to maintain the ionic gradients that underlie resting and action potentials. Although neurotransmitter regulation of the enzyme in brain has been reported, such regulation has been characterized either as a nonspecific phenomenon or as an indirect effect of neurotransmitter-induced changes in ionic gradients. We report here that the neurotransmitter dopamine, through a synergistic effect on D1 and D2 receptors, inhibits the (Na(+)+K+)ATPase activity of isolated striatal neurons. Our data provide unequivocal evidence for regulation by a neurotransmitter of a neuronal ion pump. They also demonstrate that synergism between D1 and D2 receptors, which underlies many of the electrophysical and behavioural effects of dopamine in the mammalian brain, can occur on the same neuron. In addition, the results support the possibility that dopamine and other neurotransmitters can regulate neuronal excitability through the novel mechanism of pump inhibition.     

Role of cyclic AMP in a serotonin-evoked slow inward current in snail neurones

One model of synaptic transmission suggests that transmitters modify postsynaptic permeability through the intermediary of cyclic AMP. Thus, serotonin (5-hydroxytryptamine) evokes in molluscan neurones a decrease in a voltage-dependent K+ conductance which in turn generates a slow inward current when studied in steady voltage-clamp conditions. The serotonin-induced increase of the plateau phase of the spike of an Aplysia sensory neurone can be mimicked by both intracellularly injected cyclic AMP and extracellularly applied phosphodiesterase inhibitors, suggesting that cyclic AMP mediates the effect. We have tested whether a similar mechanism could account for the serotonin slow inward current in identified snail neurones and have found that the intracellular injection of cyclic AMP, but not of cyclic GMP or 5'-AMP, evokes a slow inward current showing similar voltage dependence, inversion potential and ionic properties to the serotonin slow inward current. Phosphodiesterase inhibitors at low concentrations (1-20 microM) potentiate the serotonin slow inward current and at higher concentrations evoke by themselves an inward current, partially or totally occluding the serotonin and cyclic AMP currents. Finally, we have found that in homogenates of pooled identified snail neurones serotonin stimulates the adenylate cyclase, increasing its activity by 50-100%.     

Sodium-dependent uptake of inorganic phosphate by the intracellular malaria parasite

As the malaria parasite, Plasmodium falciparum, grows within its host erythrocyte it induces an increase in the permeability of the erythrocyte membrane to a range of low-molecular-mass solutes, including Na+ and K+ (ref. 1). This results in a progressive increase in the concentration of Na+ in the erythrocyte cytosol. The parasite cytosol has a relatively low Na+ concentration and there is therefore a large inward Na+ gradient across the parasite plasma membrane. Here we show that the parasite exploits the Na+ electrochemical gradient to energize the uptake of inorganic phosphate (P(i)), an essential nutrient. P(i) was taken up into the intracellular parasite by a Na+-dependent transporter, with a stoichiometry of 2Na+:1P(i) and with an apparent preference for the monovalent over the divalent form of P(i). A P(i) transporter (PfPiT) belonging to the PiT family was cloned from the parasite and localized to the parasite surface. Expression of PfPiT in Xenopus oocytes resulted in Na+-dependent P(i) uptake with characteristics similar to those observed for P(i) uptake in the parasite. This study provides new insight into the significance of the malaria-parasite-induced alteration of the ionic composition of its host cell.