Effects of NaCl and Ca^2＋ on Membrane Potential of Epidermal Cells of Maize Roots

The effects of salt-stress on plants involve not only the water stress caused by low osmotic pressure, but also the toxicity of excess Na^＋. A large amount of Na^＋ entering cells would reduce K^＋ uptake, which leads to an imbalance of K：Na ratio in cells. One of the reasons for the reduced K^＋-uptake is the closure of K^＋-channel which is controlled by membrane potential. Calcium is usually applied to improve the growth of plants on saline soils and shows positive influence in the integrality of cell membrane. This study applied glass microelectrode technique to monitoring the NaCl-induced changes of membrane potential of root epidermal cells of maize （Zea mays L., Denghai 11） seedlings at NaCl concentrations of 0, 8, 20, 50, 100, 200 mmol L^-1, respectively. The effect of Ca^2＋ on the changes of membrane potential caused by NaCl was also studied. The results showed that： NaCl caused cell membrane depolarization. The depolarization became greater and faster with increasing of NaCl concentration. Moreover, the extent of depolarization was positively correlated with NaCl concentration. The addition of calcium postponed the depolarization, and decreased the degree of depolarization caused by NaCl. High NaCl concentration leads to depolarization of maize root cell membrane, which can partly be counteracted by calcium.     

Residual calcium ions depress activation of calcium-dependent current

Calcium ions enter and accumulate during depolarization of some cells, activating a potassium current, IK(Ca), that depends on the cytoplasmic concentration of calcium ions, [Ca]i. However, elevation of [Ca]i can depress IK(Ca) elicited by a subsequent membrane depolarization. The depression of IK(Ca) is ascribed here to a [Ca]i-mediated inactivation of the voltage-gated calcium conductance, which causes a net reduction in calcium ions available for the activation of IK(Ca). This suggests that other processes dependent on gated calcium entry may also be depressed by small background elevations in cytosolic free calcium ions.     

Calcium dependence of the inactivation of calcium currents in skeletal muscle fibers of an insect

Calcium currents in skeletal muscle fibers of an insect, Carausius morosus, inactivate under depolarization. This inactivation depends on the current being carried across the membrane by calcium ions, rather than strontium or bariumions.     

Cyclic adenosine monophosphate: potassium-dependent action on vascular smooth muscle membrane potential

Dibutyryl cyclic adenosine monophosphate and theophylline hyperpolarize smooth muscle of rabbit main pulmonary artery in low concentrations of potassium (1 millimole per liter) but do not have a significant effect on the membrane potential in the presence of high concentrations of potassium (10 millimoles per liter). The dependence of the hyperpolarizing effect on a low external concentration of potassium is similar to that observed with isoproterenol. Prior treatment with theophylline potentiated the hyperpolarizing action of isoproterenol. These findings are compatible with the assumption that potassium-dependent, beta-adrenergic hyperpolarization is mediated by cyclic adenosine monophosphate.     

Salicylate: effect on membrane permeability of molluscan neurons

Identified cells in the buccal ganglion of the marine mollusk Navanax inermis were exposed to salicylate (1 to 30 millimoles per liter) for short periods. Salicylate increased the permneability to potassium and decreased the permeability to chloride in a reversible, dose-dependent manner, producing a concomitant increase in membrane potential and a decrease in membrane resistance. These events would reduce the output from, as well as the effectiveness of synaptic input to, a particular neuron.     

Single cell layered heart: electromechanical properties of the heart of Boltenia ovifera

The heart of Boltenia ovifera (the sea potato) is a tubular structure formed by a single layer of myocardial cells. Electron microscopic studies show that each cell contains a single myofibril located adjacent to the luminal surface of the cell. Electrical and mechanical measurement of a cannulated perfused heart demonstrate that only the luminal membrane is excitabble and elicits contraction on depolarization. Calcium and magnesium exert antagonistic effects on tension, and potassium depolarizes the myocardium and produces contractures when the luminal membrane is exposed to various concentrations of these ions. The extraluminl membrane does not respond electrically or mechanically to calcium magnesium or potassium, and its potential seems to be effectively "clamped" by the luminal membrane. Functionaly, therefore, this heart consists of a single active membrane with the adjacent contractile apparatus.     

Serum osmolality in the coelacanth, Latimeria chalumnae: urea retention and ion regulation

Samples of blood (hemolyzed) were obtained from the renal vein, the hepatic portal vein, and the heart of a freshly thawed specimen of Latimeria chalumnae. The coelacanth uses high concentrations of urea to maintain its serum osmolality at approximately that of sea water. The mean value for the total osmolality was 1181 milliosmoles per liter. The mean values (milliequivalents per liter) were: for sodium, 181; for potassium, 51.3; for calcium, 6.9; for magnesium, 28.7; for chloride, 199; and for bicarbonate, 4.7. The mean urea concentration was 355 millimoles per liter, and the mean nonprotein nitrogen was 1343 milligrams percent. Heart blood showed significantly lower values for osmolality (921 milliosmoles per liter) and nonprotein nitrogen (1030 mg percent) and was probably less severely contaminated with products of protein breakdown. Fluid from the anterior chamber of the eye showed values of 952 milliosmole/liter; the urea value for this fluid was 303 mmole/liter, and the magnesium was 7.3 meq/liter. The magnesium value for the aqueous humor was used to correct the abnormally high concentrations in the hemolyzed serum. The high level of serum potassium also was attributed to hemolysis.     

Sodium-coupled sugar transport: effects on intracellular sodium activities and sodium-pump activity

Intracellular sodium activities, (Na)c, were determined in Necturus small intestine before and after addition of galactose to the mucosal bathing solution. In the absence of galactose, (Na)c averaged 12 millimoles per liter. Within 2 minutes after the addition of galactose to the mucosal solution, (Na)c increased to a mean value of 20 millimoles per liter and then declined, in parallel with an increase in transcellular sodium transport, to a value that did not differ significantly from that observed in the absence of the sugar. The final steady state in the presence of galactose was characterized by a three- to fourfold increase in the rate of transcellular Na+ transport in the absence of a significant increase in (Na)c. Thus, the increase in steady-state basolateral pump activity cannot be attributed to an increase in the intracellular sodium transport pool.     

Ammonium and chloride extrusion: hyperpolarizing synaptic inhibition in spinal motoneurons

The reversal potential of postsynaptic inhibition shifts toward resting membrane potentials in cat spinal motoneurons after intravenous infusion of ammonium salts(1 to 3 millimoles per kilogram of body weight). Simultaneously, the depolarizing action of intracellularly injected chloride ions on the inhibitory membrane is enhanced and recovery therefrom is prolonged. Passive membrane properties remain unaltered. The results indicate a blocking of active extrusion of chloride which normally maintains a high ionic gradient for hyperpolarizing inhibition.     

A conducting polymer film stronger than aluminum

Polythiophene (Pth) was electrochemically deposited onto stainless steel substrate from freshly distilled boron fluoride-ethyl ether containing 10 millimoles of thiophene per liter. The free-standing Pth film obtained at an applied potential of 1.3 volts (versus Ag/AgCl) had a conductivity of 48.7 siemens per centimeter. Its tensile strength (1200 to 1300 kilograms per square centimeter) was greater than that of aluminium (1000 to 1100 kilograms per square centimeter). This Pth film behaves like a metal sheet and can be easily cut into various structures with a knife or a pair of scissors.     

Ionic mechanisms controlling behavioral responses of paramecium to mechanical stimulation

A mechanical stimulus applied to the anterior part of Paramecium causes a transient increase in membrane permeability to calcium. This permits a calcium current to flow into the cell, causing the membrane potential to approach the equilibrium level for calcium. The transient depolarization which results elicits a reversal in the direction of ciliary beat. When the organisms are free-swimming this is seen as the reversed locomotion of Jennings' "avoiding reaction." In contrast, a mechanical stimulus applied to the posterior part results in increased permeability to potassium ions, and hence an outward potassium current. The hyperpolarization which results causes an increase in the frequency of ciliary beat in the normal direction. In free-swimming specimens this is seen as an increase in the velocity of forward locomotion.     

Occurrence of peptide and clavine ergot alkaloids in tall fescue grass

Evidence is presented that ergot alkaloids are ubiquitous in tall fescue pastures infected with the clavicipitaceous fungal endophyte Sphacelia typhina (or Acremonium coenophialum). Ergopeptide alkaloids, predominantly ergovaline, constituted 10 to 50 percent of the total ergot alkaloid concentration, which was as high as 14 milligrams per kilogram in sheaths and 1.5 milligrams per kilogram in blades. Ergot alkaloid concentrations were substantially increased by application of large amounts (10 millimoles per liter) of potassium nitrate or ammonium chloride to infected plants in the greenhouse. The results indicate that ergot alkaloids are probably responsible for the toxicity to cattle of this common pasture and lawn grass and that ergotism-like toxicoses may be caused by clavicipitaceous fungi other than Claviceps.     

Sodium and potassium activities in normal and "sodium-rich" frog skeletal muscle

In frog sartorius muscles immersed for 2 hours at 26 degrees C in normal Ringer solution, the intrafiber potassium concentration, C(K)(in millimoles per liter), was 123 +/- 2 (mean value plus or minus standard error), and the potassium activity, a(K) (in millimoles per liter), was 90 +/- 1.0. The corresponding sodium concentration and activity were 20 +/- 1 and 6.5 +/- 0.4, respectively. After overnight immersion in K+-free Ringer solution the values were: CK, 97 +/- 2; aK, 81.5 +/- 1.6; CNa, 47 +/- 2; and aNa, 11.2 +/- 0.6. The changes in aK and aNa during storage were not consistent with an exchange between predominantly "free" fiber K+ and external Na+. These results suggest that the Na+ taken up during overnight immersion largely replaced adsorbed or sequestered K+ in the fibers.     

Cilia: activation coupled to mechanical stimulation by calcium influx

Ciliated epithelial cells in the oviduct of Necturus maculosus were stimulated mechanically by brief dimpling with a microstylus. This treatment produlced a transient depolarization of the membrane, and a transient increase in the frequency of ciliary beating. The increase in frequency of ciliary beating was related to the concentration of extracellular calcium ion, decreasing with reductiotn in calcium. Addition of lanthanum was followed by a decrease in spontaneous ciliary aictivity and a hyperpolarization of the membrane. In the presence of lanthanum, the transietnt depolarization in response to mechanical stimulation had a shorter timte course, and the concomitant increase in ciliary frequency was greatly reduced. It is concluded that calciuml ions enter the cell as a result of mechanical stimulationi of the membrane, and that calcium influx leads to an increase in the frequency of ciliary activity.     

Sodium current-induced release of calcium from cardiac sarcoplasmic reticulum

The role of sodium-calcium exchange at the sarcolemma in the release of calcium from cardiac sarcoplasmic reticulum was investigated in voltage-clamped, isolated cardiac myocytes. In the absence of calcium entry through voltage-dependent calcium channels, membrane depolarization elicited release of calcium from ryanodine-sensitive internal stores. This process was dependent on sodium entry through tetrodotoxin-sensitive sodium channels. Calcium release under these conditions was also dependent on extracellular calcium concentration, suggesting a calcium-induced trigger release mechanism that involves calcium entry into the cell by sodium-calcium exchange. This sodium current-induced calcium release mechanism may explain, in part, the positive inotropic effects of cardiac glycosides and the negative inotropic effects of a variety of antiarrhythmic drugs that interact with cardiac sodium channels. In response to a transient rise of intracellular sodium, sodium-calcium exchange may promote calcium entry into cardiac cells and trigger sarcoplasmic calcium release during physiologic action potentials.     

Tetrodotoxin and manganese ion: effects on action potential of the frog heart

Tetrodotoxin, which effectively suppresses the permeability of various tissues to sodium ions, has no effect on the calcium action potential of the fiber of barnacle muscle, which potential is produced by increase in permeability to calcium ions. Manganese ions, however, suppress the action potential. When applied to fiber of frog cardiac ventricle, tetrodotoxin suppresses the rate of rise of the action potential without affecting the overshoot; the suppressive effect of manganese ion is mainly on the overshoot of the action potential. This suggests that, in the action potential of the car-diac ventricle of the frog, the platealu phase is related primarily to the increase in permeability of the membrane to calcium ions.     

Mediation of responses to calcium in taste cells by modulation of a potassium conductance

Calcium salts are strong taste stimuli in vertebrate animals. However, the chemosensory transduction mechanisms for calcium are not known. In taste buds of Necturus maculosus (mud puppy), calcium evokes depolarizing receptor potentials by acting extracellularly on the apical ends of taste cells to block a resting potassium conductance. Therefore, divalent cations elicit receptor potentials in taste cells by modulating a potassium conductance rather than by permeating the cell membrane, the mechanism utilized by monovalent cations such as sodium and potassium ions.     

The calcium store sensor, STIM1, reciprocally controls Orai and CaV1.2 channels

Calcium signals, pivotal in controlling cell function, can be generated by calcium entry channels activated by plasma membrane depolarization or depletion of internal calcium stores. We reveal a regulatory link between these two channel subtypes mediated by the ubiquitous calcium-sensing STIM proteins. STIM1 activation by store depletion or mutational modification strongly suppresses voltage-operated calcium (Ca(V)1.2) channels while activating store-operated Orai channels. Both actions are mediated by the short STIM-Orai activating region (SOAR) of STIM1. STIM1 interacts with Ca(V)1.2 channels and localizes within discrete endoplasmic reticulum/plasma membrane junctions containing both Ca(V)1.2 and Orai1 channels. Hence, STIM1 interacts with and reciprocally controls two major calcium channels hitherto thought to operate independently. Such coordinated control of the widely expressed Ca(V)1.2 and Orai channels has major implications for Ca(2+) signal generation in excitable and nonexcitable cells.     

Adenohypophysial transmembrane potentials: polarity reversal by elevated external potassium ion concentration

Incubation of rat adenohypophyses in potassium ion of sufficient concentration to provoke the release of several of the adenohypophysial trophic hormones produces a reversed, positive transmembrane potential in more than half the cells. This finding is consistent with a process of "stimulus-secretion coupling" in which hypothalamic releasing factors act by selective depolarization of their "target" cells. The positive potentials may be due to a prolonged preferential permeability to calcium ions triggered by an initial depolarization of the cell membrane to a threshold value by increased external potassium ion.     

Electrical phenomena associated with the activity of the membrane-bound acetylcholinesterase

Treatment of isolated electroplax with physiological solutions supplemented with either 1 molar sodium chloride, 2 molar urea, or 2 molar sucrose renders the cell insensitive to carbamylcholine, phenyltrimethylammonium, or decamethonium even at high concentrations. The treated cells have a residual resting potential of -20 +/- 10 millivolts (negative inside) and are depolarized by acetylcholine at concentrations larger than 10(-3) mole per liter. This response is not affected by d-tubocurarine but is blocked by physostigmine, diisopropylphosphorofluoridate, or strong buffers and thus depends on the catalytic activity of the membrane-bound acetylcholinesterase.