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1.
用膜片钳技术中的细胞贴附方式和内面向外方式,首次在新生大鼠大脑皮层星形神经元胞体膜上记录到一类电压依赖性钾通道。此通道可被20mmol/LTEA,5mmol/LBa2+,140mmol/LCs+阻断,不受20mmol/L4—AP影响,其激活不依赖Ca2+。膜外钾离子浓度对通道的特性有显著的影响,逆转电位随[K+]0的增大而增大,并表现出一定的饱和现象,两者的对数呈线性关系;同一驱动电位下,平均开放时间和开放概率随[K+]0的增大而增大,平均关闭时间的变化则相反。  相似文献   

2.
LHRH—A2及无机离子促进草鱼脑垂体离体分泌GH的初步研究   总被引:1,自引:0,他引:1  
用培养瓶(皿)培养法研究LHRH-A2、Ca^2+、K^+对草鱼脑垂体器官分泌GH的影响。结果表明,1nmol/L、10nmol/L、100nmol/L和1000nmol/L的LHRH-A2都能显著促进GH的分泌;随着Ca^2+浓度(0.1、1、3mmol/L)的增高GH的分泌增强,在1mol/L和3mmol/L Ca^2+条件下的GH分泌水平显著高于在0.1mmol/L Ca^2+条件下的GH分  相似文献   

3.
研究了铝和铝+_钙对小麦功苗根尖质膜、液泡膜微囊H^+-ATP酶、Ca^2+-ATP酶、Mg^2+-ATP酶活性及共动力学参数和膜流动性的影响。在质膜和液泡膜微囊制剂中加入1.0mmol/L的AI^3+(AICI3)时,H^2+-ATP囊制剂中加入1.0mmol/L的AI^3+(AICI3)时,H^+-ATP酶、Ca^2+-ATP酶、Mg^2+-ATP酶活笥和酶促反应的Vmax及膜流动性下降,而酶  相似文献   

4.
钙离子对江浙蝮蛇毒酸性磷脂酶A2结构与功能的影响   总被引:5,自引:0,他引:5  
张翔  郑乐 《生物化学杂志》1994,10(3):330-334
钙离子在江浙蝮蛇毒酸性磷脂酶A2中的作用是多方面的,它不仅能够引起酸性磷脂酶A2在溶液中构象的变化,而且对该酶活性有较大的影响,Ca^2+为酶活力所必需,当Ca^2+浓度达到0.06mmol/L时,酶表现出很的活力;Ca^2+浓度超过0.5mmol/L时,催化反应出现一个明显的延滞期。化学修饰表明His47在表现活力方面起重要作用,Ca^2+的存在可降低其修饰反应的速度,提示这是由于Ca^2+引起  相似文献   

5.
20~100μmol.l^-1外源亚精胺(Spd)抑制苹果(品种:国光、富士、金冠)花粉萌发与花粉管伸长,其效应随浓度增加而增强;Ca^2+(1mmol.L^-1)在一定程度上削弱这种抑制效应,而Ca^2+的良好作用则又为Ca^2+通道竞争性抑制剂La^2+所消除,Ca^2+载体A23187仅削弱Ca^2+对花粉管 工的良好作用。  相似文献   

6.
研究了铝胁迫下耐铝性不同的两个小麦品种根细胞液泡膜ATP酶、焦磷酸酶活性和膜脂的变化。与对照相比,经20和100mol/L的AlCl3处理后,耐铝品种Altas66的液泡膜H^+-ATP和和Ca^2+-ATP酶活性迅速下降;铝敏感品种Scout66液泡膜H^+-ATP酶和Ca^2+-ATP酶活性则在20μmol/L时增加,100μmol/L时下降。焦磷酸酶活性在Al-tas66中下降,在Scout  相似文献   

7.
10μg/g的IAA溶液强烈地促进玉米胚芽鞘切段的延长生长和质子分泌,但这两种效应的启动时间有别.Ca2+在高浓度下(2—5mmol/L)强烈抑制IAA诱导的延长生长,但在低浓度下(0.5mmol/L)则有轻微的促进作用.IAA增大质膜相对透性,而Ca2+则有稳定膜的作用,且适宜的浓度较低(0.5mmol/L).  相似文献   

8.
重组于脂双层的人精子质膜Ca2+通道的膜片箝研究   总被引:5,自引:0,他引:5  
Ma XH  Shi YL 《生理学报》1999,51(5):571-579
跨膜离子流动在启动配子间的相互作用,如顶体反应过程中有重要作用。.但由于精子太小,无用论细胞内记录或膜片箝技术都难以对哺乳动物精子膜的离子通病进行研究。本工作将通道蛋白重组于脂双层,在电压箝位下记录了人精子膜的Ca^2+通道电流。由12个健康人的精子分离的膜蛋白通过融合重组于脂双层后,在CaCl2溶液中(cis50//trans 10mmol/L)记录到两类单通道活动,它们的平衡电位都接近Ca^2  相似文献   

9.
G蛋白在亮啡肽诱导心肌细胞内钙释放中的作用   总被引:1,自引:0,他引:1  
魏振宇  谈世进 《生理学报》1995,47(2):173-178
本实验采用分离的SD大鼠心室肌细胞,以Fura-2AM荧光指示剂负载,检测心肌细胞内游离钙浓度(Ca^2+)变化。探讨亮啡肽(LEK)对(Ca^2+)的作用及其机制。实验结果:LEK(60μmol/L)能升高(Ca^2+)移去细胞外液钙此效应仍能出现,用caffeine (5mmol/L)耗竭细胞内钙池的钙,该效应消失,纳洛酮(100μmol/L),百日咳毒素(200ng/L)处理8-10h及pr  相似文献   

10.
介质Ca^2+和La^3+对酿酒酵母生长的影响   总被引:8,自引:0,他引:8  
采用正交实验研究了外加Ca^2+和La^3+对酿酒酵母生长的影响。结果表明:外加Ca^2+和La^3+对酿酒酵母的生长均有显的影响,都呈现出低浓度对正效应和高浓度时负效应,当Ca^2+浓度为1mmol/L及La^3+浓度为15μmol/L时酿酒酵母生长最好。  相似文献   

11.
Currents through single potassium channels were studied in cell-attached or inside-out patches from collagenase-dispersed smooth muscle cells of the guinea pig taenia coli. Under conditions mimicking the physiological state with [K+]i = 135 mM: [K+]o = 5.4 mM, three distinct types of K+ channel were identified with conductances around 0 mV of 147, 94, and 63 pS. The activities of the 94- and 63-pS channel were observed infrequently. The 147-pS channel was most abundant. It has a reversal potential of approximately -75 mV. It is sensitive to [Ca2+]i and to membrane potential. At -30 mV, the probability of a channel being open is at a minimum. At more positive voltages, the probability follows Boltzman distribution. A 10-fold change in [Ca2+]i causes a 25-mV negative shift of the voltage where half of the channels are open; an 11.3-mV change in membrane potential produces an e-fold increase in the probability of the channel being open when P is low. At voltages between -30 and -50 mV, the open probability increases in an anomalous manner because of a large decrease of the channel closed time without much change in the channel open time. This anomalous activity may play a regulatory role in maintaining the resting potential. The histograms of channel open and closed time fit well, respectively, with single and double exponential distributions. Upon step depolarizations by 100-ms pulses, the 147-pS channel opens with a brief delay. The delay shortens and both the number of open channels and the open time increase with increasing positivity of the potential. The averaged currents during the step depolarizations closely resemble the delayed rectifying outward K+ currents in whole-cell recordings.  相似文献   

12.
Chen KY  Zhu PH 《生理学报》1999,(2):153-160
用蛙胫前肌小束为材料, 研究了提高胞外钾[K+]O对咖啡因挛缩的作用.[K+]O从2 mmol/L提高到10或25 mmol/L, 由3 mmol/L咖啡因引起的挛缩明显增强.以PKC/PC (PKC和PC分别为在高钾和正常钾条件下的咖啡因挛缩)表示的咖啡因挛缩增强, 依赖[K+]O和高钾作用时间.随着10 mmol/L [K+]O作用时间延长, 直至10 min, 增强逐渐增加.但是, 25 mmol/L [K+]O作用1 min时增强达到最大, 然后下降到对照.PKC/PC变化时程不能用高钾引起的去极化解释, 而与由相似[K+]O引起的胞浆自由钙变化时程相符.提示, 至少在蛙骨骼肌, 高钾引起的咖啡因挛缩增强主要是由胞浆自由钙升高引起的.  相似文献   

13.
三羟异黄酮对豚鼠心室肌细胞内游离钙浓度的影响   总被引:3,自引:0,他引:3  
Ji ES  Wang C  He RR 《生理学报》2004,56(2):204-209
用激光共聚焦显微镜观察研究三羟异黄酮(genistein,GST)对豚鼠心室肌细胞内游离钙浓度([Ca^2 ]i)的影响。结果用相对荧光强度(FI-F0/FX0,%)表示。实验结果显示,在正常台氏液、无钙台氏液和正常台氏液中加入3mmol/L EGTA后,GST(10~40μmol/L)浓度依赖性地降低细胞内钙浓度。蛋白酪氨酸磷酸酶抑制剂正钒酸钠(sodium orthovanadate)和L-型Ca^2 通道激动剂Bay K8644可部分抑制正常台氏液时GST的效应。当细胞外液钙浓度由1mmol/L增加到10mmol/L而诱发心室肌细胞钙超载时,部分心室肌细胞产生可传播的钙波,GST(40μmol/L)可降低钙波的传播速度和持续时间,最终阻断钙波。以上结果提示,GST降低心室肌细胞内游离钙浓度,此作用与其抑制电压依赖性Ca^2 通道、减弱酪氨酸激酶抑制和豚鼠心室肌细胞肌浆网内钙释放有关。  相似文献   

14.
Ca2(+)-sensitive K+ channel in aortic smooth muscle of rats   总被引:2,自引:0,他引:2  
We measured K+ channel activity in inside-out patches of cell membrane from aortic vascular smooth muscle cultured (Passages 1-3) from Wistar, Wistar-Kyoto, and spontaneously hypertensive rats (SHR). With [Ca2+]i between 25 and 100 nm and 150 mm K+ on both sides of the membrane, the conductance of this channel was 55 +/- 7 pS (slope of current-voltage curve through 0 mV) and the current was outwardly rectified. There was no difference in single-channel conductance among the three rat strains. Increasing negative holding voltages or increasing [Ca2+]i, increased the probability of this type channel being open (Npo; P less than 0.01); SHR had a larger NPo (P less than 0.01). Compared with cells from Wistar and Wistar-Kyoto, cells from SHR also had the longest mean open time. The increased NPo and mean open time we observed in this K+ channel of cells from SHR could contribute, at least in part, to the increased membrane K+ permeability, reported previously.  相似文献   

15.
Extracellular potassium modulates recovery from C-type inactivation of Kv1.3 in human T lymphocytes. The results of whole-cell patch clamp recordings show that there is a linear increase in recovery rate with increasing [K+]o. An increase from 5 to 150 mM K+o causes a sixfold acceleration of recovery rate at a holding potential of -90 mV. Our results suggest that 1) a low-affinity K+ binding site is involved in recovery, 2) the rate of recovery increases with hyperpolarization, 3) potassium must bind to the channel before inactivation to speed its recovery, and 4) recovery rate depends on external [K+] but not on the magnitude of the driving force through open channels. We present a model in which a bound K+ ion destabilizes the inactivated state to increase the rate of recovery of C-type inactivation, thereby providing a mechanism for autoregulation of K+ channel activity. The ability of K+ to regulate its own conductance may play a role in modulating voltage-dependent immune function.  相似文献   

16.
Extracellular [K+] can increase during some pathological conditions, resulting into excessive glutamate release through multiple mechanisms. We here investigate the overflow of [3H]D-aspartate ([3H] D-ASP) and of endogenous glutamate elicited by increasing [K+] from purified rat cerebrocortical synaptosomes. Depolarization with [K+] 15 mmol/L were prevented by the glutamate transporter inhibitors DL-threo-beta-benzyloxyaspartate (DL-TBOA) and dihydrokainate. Differently, the overflows of endogenous glutamate provoked by [K+] > 15 mmol/L were insensitive to both inhibitors; the external Ca2+-independent glutamate overflow caused by 50 mmol/L KCl was prevented by bafilomycin, by chelating intraterminal Ca2+, by blocking the mitochondrial Na+/Ca2+ exchanger and, for a small portion, by blocking anion channels. In contrast to purified synaptosomes, the 50 mmol/L K+-evoked release of endogenous glutamate or [3H]D-ASP was inhibited by DL-TBOA in crude synaptosomes; moreover, it was external Ca2+-insensitive and blocked by DL-TBOA in purified gliosomes, suggesting that carrier-mediated release of endogenous glutamate provoked by excessive [K+] in CNS tissues largely originates from glia.  相似文献   

17.
The effect of pH on the activation of a Ca-activated K+ [K(Ca)] channel from rat skeletal muscle incorporated into planar lipid bilayers was studied. Experiments were done at different intracellular Ca2+ and proton concentrations. Changes in pH modified channel kinetics only from the Ca-sensitive face of the channel. At constant Ca2+ concentration, intracellular acidification induced a decrease in the open probability (Po) and a shift of the channel activation curves toward the right along the voltage axis. The displacement was 23.5 mV per pH unit. This displacement was due to a change in the half saturation voltage (Vo) and not to a change in channel voltage dependence. The shifts in Vo induced by protons appeared to be independent of Ca2+ concentration. The slope of the Hill plot of the open-closed equilibrium vs. pH was close to one, suggesting that a minimum of one proton is involved in the proton-driven channel closing reaction. The change in Po with variations in pH was due to both a decrease in the mean open time (To) and an increase in the mean closed time (Tc). At constant voltage, the mean open time of the channel was a linear function of [Ca2+] and the mean closed time was a linear function of 1/[Ca2+]2. Changes in the internal pH modified the slope, but not the intercept of the linear relations To vs. [Ca2+] and Tc vs. 1/[Ca2+]2. On the basis of these results an economical kinetic model of the effect of pH on this channel is proposed. It is concluded that protons do not affect the open-closed reaction, but rather weaken Ca2+ binding to all the conformational states of the channel. Moreover, competitive models in which Ca2+ and H+ cannot bind to the same open or closed state are inconsistent with the data.  相似文献   

18.
Outward currents through inward rectifier K+ channels (Kir) play a pivotal role in determining resting membrane potential and in controlling excitability in many cell types. Thus, the regulation of outward Kir current (IK1) is important for appropriate physiological functions. It is known that outward IK1 increases with increasing extracellular K+ concentration ([K+]o), but the underlying mechanism is not fully understood. A "K+-activation of K+-channel" hypothesis and a "blocking-particle" model have been proposed to explain the [K+]o-dependence of outward IK1. Yet, these mechanisms have not been examined at the single-channel level. In the present study, we explored the mechanisms that determine the amplitudes of outward IK1 at constant driving forces [membrane potential (Vm) minus reversal potential (EK)]. We found that increases in [K+]o elevated the single-channel current to the same extent as macroscopic IK1 but did not affect the channel open probability at a constant driving force. In addition, spermine-binding kinetics remained unchanged when [K+]o ranged from 1 to 150 mM at a constant driving force. We suggest the regulation of K+ permeation by [K+]o as a new mechanism for the [K+]o-dependence of outward IK1.  相似文献   

19.
The interaction of Ca2+ and Ba2+ with a Ca2+-activated K+ channel from rabbit skeletal muscle membranes is studied in planar lipid bilayers. At [Ca2+] greater than or equal to 100 microM in the cis side (the side to which the vesicles are added) and at positive voltages, the channel kinetics consisted of bursts of activity interrupted by long periods of quiescence. We found that the reciprocal of the mean burst time increases linearly with [Ca2+], whereas the mean time for the quiescent (closed) periods is independent of [Ca2+]. The number of quiescent periods is reduced by increasing [K+]. Micromolar amounts of cis Ba2+ do not activate the channel, but induce similar "slow" closings. Also, in this case, the mean burst time is inversely proportional to the [Ba2+] and the mean closed time is independent of [Ba2+]. Raising [K+] either symmetrically or only in the trans side relieved the Ba2+ effect. trans Ba2+ also induces changes in the slow kinetics, but in millimolar amounts. These results suggest that the quiescent periods correspond to a channel blocked by a Ba ion. The voltage dependence of the cis blockade indicates that the Ba2+ binding site is past the middle of the membrane field. The similarities in the slow kinetics induced by Ca2+ and Ba2+ suggest that Ca2+ blocks the channel by binding to the same site. However, binding of Ca2+ to the site is 10(5)- fold weaker.  相似文献   

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