Journal articles: 'Cationic conductance'

1

Wang, Hong-Zhan, and Richard D. Veenstra. "Monovalent Ion Selectivity Sequences of the Rat Connexin43 Gap Junction Channel." Journal of General Physiology 109, no. 4 (April 1, 1997): 491–507. http://dx.doi.org/10.1085/jgp.109.4.491.

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The relative permeability sequences of the rat connexin 43 (rCx43) gap junction channel to seven cations and chloride were examined by double whole cell patch clamp recording of single gap junction channel currents in rCx43 transfected neuroblastoma 2A (N2A) cell pairs. The measured maximal single channel slope conductances (γj, in pS) of the junctional current-voltage relationships in 115 mM XCl were RbCl (103) ≥ CsCl (102) > KCl (97) > NaCl (79) ≥ LiCl (78) > TMACl (65) > TEACl (53) and for 115 mM KY were KBr (105) > KCl (97) > Kacetate (77) > Kglutamate (61). The single channel conductance-aqueous mobility relationships for the test cations and anions were linear. However, the predicted minimum anionic and cationic conductances of these plots did not accurately predict the rCx43 channel conductance in 115 mM KCl. Instead, the conductance of the rCx43 channel in 115 mM KCl was accurately predicted from cationic and anionic conductance-mobility plots by applying a mobility scaling factor Dx/Do, which depends upon the relative radii of the permeant ions to an estimated pore radius. Relative permeabilities were determined for all of the monovalent cations and anions tested from asymmetric salt reversal potential measurements and the Goldman-Hodgkin-Katz voltage equation. These experiments estimate the relative chloride to potassium permeability to be 0.13. The relationship between the relative cation permeability and hydrated radius was modeled using the hydrodynamic equation assuming a pore radius of 6.3 ± 0.4 Å. Our data quantitatively demonstrate that the rCx43 gap junction channel is permeable to monovalent atomic and organic cations and anions and the relative permeability sequences are consistent with an Eisenman sequence II or I, respectively. These predictions about the rCx43 channel pore provide a useful basis for future investigations into the structural determinants of the conductance and permeability properties of the connexin channel pore.

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Tsunenari, T., Y. Hayashi, M. Orita, T. Kurahashi, A. Kaneko, and T. Mori. "A quinine-activated cationic conductance in vertebrate taste receptor cells." Journal of General Physiology 108, no. 6 (December 1, 1996): 515–23. http://dx.doi.org/10.1085/jgp.108.6.515.

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The chincona alkaloid quinine is known to be a bitter tasting substance for various vertebrates. We examined the effects of quinine on isolated taste receptor cells from the bullfrog (Rana catesbeiana). Membrane currents were recorded by whole-cell recording, while quinine hydrochloride was applied extracellularly from a puffer pipette. At the resting potential (-77 +/- 9 mV, mean +/- SD, n = 49 cells), taste cells generated inward currents in response to quinine stimulation (> 1 mM), indicating a depolarizing response in the taste cells. Two types of current responses were observed; a newly found quinine-activated cationic conductance and a previously reported blocking effect of quinine on K+ conductances. The cationic current was isolated from the K+ current by using a Cs(+)-containing patch pipette. The relative permeabilities (Pion) of the quinine-activated cationic conductance were: PNa/PK/PCs = 1:0.5:0.42. The quinine dose-response relation was described by the Hill equation with the K1/2 of 3.6 mM and Hill coefficient of 5.3. When extracellular [Ca2+] (1.8 mM) was reduced to nominally free, the conductance was enhanced by about sixfold. This property is consistent with observations on quinine responses recorded from the gustatory nerve, in vivo. The quinine-induced cationic current was decreased with an application of 8-bromo-cAMP. We conclude that the bitter substance quinine activates a cation channel in taste receptor cells and this channel plays an important role in bitter taste transduction.

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Tzan, C. J., J. R. Berg, and S. A. Lewis. "Modification of epithelial permeability by cationic polypeptides." American Journal of Physiology-Cell Physiology 265, no. 6 (December 1, 1993): C1637—C1647. http://dx.doi.org/10.1152/ajpcell.1993.265.6.c1637.

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It has been demonstrated that protamine sulfate (PS; a cationic polypeptide composed of 70% arginine) increases the apical membrane conductance of the mammalian urinary bladder. In this report, synthetic cationic polypeptides (CpP; e.g., polyarginine) were used to determine whether the response of the bladder to PS was due to its cationic nature (i.e., its arginine content). We demonstrate that CpP induce a large increase in the cation and anion conductance of the apical membrane of the rabbit urinary bladder epithelium. The modulation of the membrane conductance by CpP is dependent upon a number of parameters. 1) The magnitude of the conductance change was voltage dependent. 2) An increase in the total charge per molecule increased the rate of conductance change. 3) An increase in the charge density (ratio of charged amino acids to total amino acids) increased the rate of change of conductance. 4) La3+ inhibited the ability of CpP to alter the membrane conductance. 5) The rate of reversal of the CpP-induced conductance was dependent upon the total charge per molecule as well as the charge density. 6) The level of self-inhibition (ability of solution CpP to inhibit the CpP-induced membrane conductance) was inversely correlated with the charge density and was also concentration dependent, with less inhibition occurring at low mucosal CpP concentrations. These data are consistent with a model developed to describe the effect of PS on the conductive properties of the urinary bladder epithelium.

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Tzan, C. J., J. R. Berg, and S. A. Lewis. "Mammalian urinary bladder permeability is altered by cationic proteins: modulation by divalent cations." American Journal of Physiology-Cell Physiology 267, no. 4 (October 1, 1994): C1013—C1026. http://dx.doi.org/10.1152/ajpcell.1994.267.4.c1013.

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It was previously demonstrated that protamine sulfate (PS, a cationic polypeptide) as well as synthetic cationic polypeptides (CpP, e.g., polylysine and polyarginine) caused an increase in the apical membrane conductance of the mammalian urinary bladder epithelium that was voltage dependent. The membrane conductance induced by these CpP was mediated by a saturable binding site and was partially blocked by CpP (self-inhibition). The PS-induced membrane conductance can be modified by polyvalent cations at three sites. The first site was to competitively inhibit the interaction of PS with an apical membrane binding site. The second site was to reversibly block the conductance induced by PS. The relative binding affinity (block of PS-induced conductance) sequence was as follows: UO2(2+) > La3+ > Mn2+ > Ba2+ > or = Ca2+ > Sr2+. Although La3+, Mn2+, Ba2+, Ca2+, and Sr2+ inhibited > or = 81% of the PS-induced conductance, UO2(2+) inhibited only 51% and Mg2+ was without effect. The third site was to increase the rate of loss of the PS-induced conductance from the apical membrane. Although neither carbodiimides (carboxyl group reactive reagents) nor neuraminidase (cleaves sialic acid residues) altered the effect of PS on the urinary bladder conductance, PS increased the conductance of lipid bilayers composed of negatively charged phospholipids. A candidate for the binding site might be the negatively charged phosphate groups of membrane lipids.

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5

Fologea, Daniel, Eric Krueger, Steve Rossland, Sheenah Bryant, Wylie Foss, and Tyler Clark. "Cationic Polymers Inhibit the Conductance of Lysenin Channels." Scientific World Journal 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/316758.

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The pore-forming toxin lysenin self-assembles large and stable conductance channels in natural and artificial lipid membranes. The lysenin channels exhibit unique regulation capabilities, which open unexplored possibilities to control the transport of ions and molecules through artificial and natural lipid membranes. Our investigations demonstrate that the positively charged polymers polyethyleneimine and chitosan inhibit the conducting properties of lysenin channels inserted into planar lipid membranes. The preservation of the inhibitory effect following addition of charged polymers on either side of the supporting membrane suggests the presence of multiple binding sites within the channel's structure and a multistep inhibition mechanism that involves binding and trapping. Complete blockage of the binding sites with divalent cations prevents further inhibition in conductance induced by the addition of cationic polymers and supports the hypothesis that the binding sites are identical for both multivalent metal cations and charged polymers. The investigation at the single-channel level has shown distinct complete blockages of each of the inserted channels. These findings reveal key structural characteristics which may provide insight into lysenin’s functionality while opening innovative approaches for the development of applications such as transient cell permeabilization and advanced drug delivery systems.

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6

Zholos, A. V., and T. B. Bolton. "Effects of protons on muscarinic receptor cationic current in single visceral smooth muscle cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 2 (February 1, 1997): G215—G223. http://dx.doi.org/10.1152/ajpgi.1997.272.2.g215.

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Effects of extracellular protons on muscarinic receptor-evoked cationic current (Icat) in single guinea pig ileal smooth muscle cells were studied by use of patch-clamp techniques: intracellular pH and pCa were buffered to 7.4 and 7.0, respectively, symmetrical 124 mM Cs+ solutions were used, and divalent cations were removed from the bathing solution. Increasing extracellular pH (pHo) from 7.4 to 8.4 caused a 16-mV parallel negative shift of the activation curve for Icat evoked by guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS) with an increase in the maximal conductance and slowed Icat relaxation on hyperpolarization; acidification to pHo 6.4 produced equivalent but opposite effects. Carbachol- and GTPgammaS-activated Icat behaved similarly, suggesting that the cationic channel rather than the muscarinic receptor was the major site of action. From 11.4 to 4.4 pHo, maximal cationic conductance was reduced progressively, and the activation curve shifted positively. Na+, K+, Ca2+, and Mg2+ had complex interactions with pHo-induced effects considered to be attributable to interaction of protons with fixed negative surface charges and, at positive potentials, to channel block.

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7

Kleine, T. J., A. Gladfelter, P. N. Lewis, and S. A. Lewis. "Histone-induced damage of a mammalian epithelium: the conductive effect." American Journal of Physiology-Cell Physiology 268, no. 5 (May 1, 1995): C1114—C1125. http://dx.doi.org/10.1152/ajpcell.1995.268.5.c1114.

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Human semen has been reported to be cytotoxic to rat descending colon by a mechanism involving polyamines (cationic molecules) and collagenase. In this study, we report that histones, cationic proteins found in human semen, can contribute to semen's cytotoxicity. Histones H1, H4, and H5, when added to the mucosal side of rabbit urinary bladder epithelium, were found to alter the transepithelial conductance (Gt) in a voltage-sensitive manner. When the cell interior was negative, the conductance rapidly increased and plateaued. When the cell interior was positive, the induced conductance decreased to control values. Histone increased the Gt by increasing the apical membrane conductance rather than the tight junction conductance. The magnitude of the Gt increase was dose dependent, and the histone-induced conductance was nonselective for Na+, K+, and Cl-. The induced conductance could be reversed by either increasing mucosal Ca2+ concentration or by removal of histone from the mucosal solution. Prolonged exposure of the epithelium to histone was toxic as determined by the irreversible loss of transepithelial resistance. These results indicate that histone increases membrane ionic permeability, is cytotoxic, and thus may contribute to human semen's toxic effect on colonic epithelium.

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8

Queiroga, Claudiene M. de, Geovani S. de Lima, Rafaela A. F. Torres, Francisco J. da S. Paiva, Lauriane A. dos A. Soares, and Hans R. Gheyi. "Formation of guava seedlings under irrigation with water of different cationic natures and salicylic acid." Revista Caatinga 36, no. 3 (September 2023): 650–62. http://dx.doi.org/10.1590/1983-21252023v36n318rc.

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ABSTRACT The objective of this study was to evaluate gas exchange, biomass, and quality of guava seedlings as a function of the cationic nature of the water used in irrigation and foliar application of salicylic acid. The experiment was carried out in a greenhouse in Pombal, PB, Brazil, using a randomized block design, in a 6 × 4 factorial scheme with six cationic compositions of irrigation water [S1 - Control (supply water); S2 - Na+; S3 - Ca2+; S4 - Na++Ca2+; S5 - Mg2+, and S6 - Na++Ca2++Mg2+], associated with four concentrations of salicylic acid (0, 1.3, 2.6, and 3.9 mM), with 3 replicates. Plants in control (S1) were irrigated with water of electrical conductivity (ECw) of 0.3 dS m-1, while in the other treatments were irrigated with different types of water and had an ECw of 4.3 dS m-1, consisting of different cations, in the form of chloride. In the seedling formation phase, guava plants were sensitive to calcic water, which resulted in a marked decrease in their growth. Stomatal conductance, transpiration, and biomass accumulation of guava seedlings were more affected by variation in electrical conductivity than by cationic nature of the water. Salicylic acid at concentrations of 2.9 and 1.9 mM increased stomatal conductance and stem dry biomass, respectively, of guava seedlings. Water with ECw of 4.3 dS m-1 allowed the formation of guava seedlings with acceptable quality for transplanting to the field, regardless of the cationic nature of the water.

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9

Jin, Nan Ge, Sang Don Koh, and Kenton M. Sanders. "Caffeine inhibits nonselective cationic currents in interstitial cells of Cajal from the murine jejunum." American Journal of Physiology-Cell Physiology 297, no. 4 (October 2009): C971—C978. http://dx.doi.org/10.1152/ajpcell.00155.2009.

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Interstitial cells of Cajal (ICC) discharge unitary potentials in gastrointestinal muscles that constitute the basis for pacemaker activity. Caffeine has been used to block unitary potentials, but the ionic conductance responsible for unitary potentials is controversial. We investigated currents in cultured ICC from murine jejunum that may underlie unitary potentials and studied the effects of caffeine. Networks of ICC generated slow wave events under current clamp, and these events were blocked by caffeine in a concentration-dependent manner. Single ICC generated spontaneous transient inward currents (STICs) under voltage clamp at −60 mV and noisy voltage fluctuations in current clamp. STICs were unaffected when the equilibrium potential for Cl− ( ECl) was set to −60 mV (excluding Cl− currents) and reversed at 0 mV, demonstrating that a nonselective cationic conductance, and not a Cl− conductance, is responsible for STICs in ICC. Caffeine inhibited STICs in a concentration-dependent manner. Reduced intracellular Ca2+ and calmidazolium (CMZ; 1 μM) activated persistent inward, nonselective cation currents in ICC. Currents activated by CMZ and by dialysis of cells with 10 mM BAPTA were also inhibited by caffeine. Excised inside-out patches contained channels that exhibited spontaneous openings, and resulting currents reversed at 0 mV. Channel openings were increased by reducing Ca2+ concentration from 10−6 M to 10−8 M. CMZ (1 μM) also increased openings of nonselective cation channels. Spontaneous currents and channels activated by CMZ were inhibited by caffeine (5 mM). The findings demonstrate that the Ca2+-inhibited nonselective cation channels that generate STICs in ICC are blocked directly by caffeine. STICs are responsible for unitary potentials in intact muscles, and the block of these events by caffeine is consistent with the idea that a nonselective cation conductance underlies unitary potentials in ICC.

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10

Lee, H. K., C. W. Shuttleworth, and K. M. Sanders. "Tachykinins activate nonselective cation currents in canine colonic myocytes." American Journal of Physiology-Cell Physiology 269, no. 6 (December 1, 1995): C1394—C1401. http://dx.doi.org/10.1152/ajpcell.1995.269.6.c1394.

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The mechanism of tachykinin-induced excitation was studied in isolated colonic muscle cells and intact muscle strips. In whole cell voltage-clamp studies performed at 33 degrees C, neurokinin A (NKA) and substance P (SP) reduced L-type Ca2+ current. NKA and SP activated a cationic current that reversed near 0 mV. This current (INKA or ISP, respectively) had properties similar to the acetylcholine (ACh)-activated nonselective cation conductance (IACh), activated by muscarinic stimulation in other gastrointestinal smooth muscle cells. INKA and ISP were decreased when external Na+ was reduced. In contrast to IACh, INKA and ISP were not facilitated by increases in internal Ca2+, but little or no current was activated by these peptides when extracellular Ca2+ was low. INKA (10(-7) M) and ISP (10(-5) M) were blocked by Cd2+ (5 x 10(-4) M), quinine (10(-3) M), and the tachykinin-receptor antagonist [D-Pro2,D-Trp7,9]SP (10(-5) M). Current clamp recordings and intracellular recordings of intact tissues showed that NKA and SP depolarized the cell membrane, which is consistent with the activation of a nonselective cation conductance. These data suggest that a primary mechanism of the tachykinins is to activate a nonselective cation conductance that leads to depolarization. The increase in Ca2+ entry due to tachykinin stimulation appears to be secondary to the activation of the nonselective cation conductance.

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11

Oliet, S. H., and C. W. Bourque. "Steady-state osmotic modulation of cationic conductance in neurons of rat supraoptic nucleus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 6 (December 1, 1993): R1475—R1479. http://dx.doi.org/10.1152/ajpregu.1993.265.6.r1475.

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Whole cell patch-clamp recordings were obtained from isolated rat supraoptic nucleus magnocellular neurosecretory cells (MNCs). Under current clamping, hyperosmolality produced by the addition of 10-30 mM mannitol depolarized each of 25 cells tested. In contrast, reducing fluid osmolality from 295 to 265 mosmol/kgH2O had the reverse effect, hyperpolarizing 18 of 21 MNCs. Voltage-clamp recordings in 43 cells revealed that the effects of hypo- and hyperosmolality, respectively, were caused by decreases and increases in a nonselective cation conductance reversing near -41 mV. Current-voltage analysis in Na(+)-free solution revealed that the reversal potentials of currents elicited by increases and decreases in osmolality both shifted to a value near -90 mV, suggesting that a single ionic conductance is modulated by these stimuli. The relation between cationic conductance and osmolality was specific, sensitive (+2.14%.mosmol-1.kgH2O-1), and well-fit by linear regression (r = 0.96; n = 22 cells) between 275 and 325 mosmol/kgH2O. These results indicate that MNCs express a depolarizing current that is active under steady-state conditions and that the up- or downregulation of this current contributes to the excitation or inhibition of these cells upon acute exposure to hypo- or hyperosmolar conditions.

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12

Yadav, Ram Nath Prasad. "Synthesis, characterisation and reactions of cationic complexes of Arylantimony (III) chlorides ArnSbCl3-n with perchlorate and tetrafluoroborate anions." International Journal of Applied Sciences and Biotechnology 1, no. 2 (June 15, 2013): 42–48. http://dx.doi.org/10.3126/ijasbt.v1i2.8204.

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Several hitherto unreported cationic complexes of the general formula [Ar2SbL][Y] and [ArSbL2][Y]2 [ Where, Ar = C6H5, L = α-Picoline, Pyridine, Ph3AsO, hexamethyl phosphoramide (HMPA), thiourea (TU) and Y = ClO4− BF4− ] have been synthesized and characterized by solid state IR, 1H NMR, elemental analysis, conductance and molecular weight measurements. The physico-chemical data, cations [Ar2SbL]+1 and[ArSbL2]+2 are assigned a pyramidal structure.DOI: http://dx.doi.org/10.3126/ijasbt.v1i2.8204 Int J Appl Sci Biotechnol, Vol. 1(2): 42-49

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13

Palepu, Ramamurthy, and Vincent C. Reinsborough. "Surfactant–cyclodextrin interactions by conductance measurements." Canadian Journal of Chemistry 66, no. 2 (February 1, 1988): 325–28. http://dx.doi.org/10.1139/v88-056.

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Conductance measurements were used to identify and to obtain association constants for the complexes formed between cyclodextrins (CD) with emphasis on β-cyclodextrin (βCD), and surfactants such as sodium dodecylsulfate (SDS) and tetradecyltrimethyl ammonium bromide. With both anionic and cationic surfactants, αCD forms predominantly a 2:1 CD/surfactant complex while with both βCD and γCD the main species is 1:1. γCD binds much less strongly with surfactants than both αCD and βCD. Cyclodextrins destroy micelles by complexing the surfactant monomers more strongly than they are bound in self-association.

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14

Smith, J. S., T. Imagawa, J. Ma, M. Fill, K. P. Campbell, and R. Coronado. "Purified ryanodine receptor from rabbit skeletal muscle is the calcium-release channel of sarcoplasmic reticulum." Journal of General Physiology 92, no. 1 (July 1, 1988): 1–26. http://dx.doi.org/10.1085/jgp.92.1.1.

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The ryanodine receptor of rabbit skeletal muscle sarcoplasmic reticulum was purified as a single 450,000-dalton polypeptide from CHAPS-solubilized triads using immunoaffinity chromatography. The purified receptor had a [3H]ryanodine-binding capacity (Bmax) of 490 pmol/mg and a binding affinity (Kd) of 7.0 nM. Using planar bilayer recording techniques, we show that the purified receptor forms cationic channels selective for divalent ions. Ryanodine receptor channels were identical to the Ca-release channels described in native sarcoplasmic reticulum using the same techniques. In the present work, four criteria were used to establish this identity: (a) activation of channels by micromolar Ca and millimolar ATP and inhibition by micromolar ruthenium red, (b) a main channel conductance of 110 +/- 10 pS in 54 mM trans Ca, (c) a long-term open state of lower unitary conductance induced by ryanodine concentrations as low as 20 nM, and (d) a permeability ratio PCa/PTris approximately equal to 14. In addition, we show that the purified ryanodine receptor channel displays a saturable conductance in both monovalent and divalent cation solutions (gamma max for K and Ca = 1 nS and 172 pS, respectively). In the absence of Ca, channels had a broad selectivity for monovalent cations, but in the presence of Ca, they were selectively permeable to Ca against K by a permeability ratio PCa/PK approximately equal to 6. Receptor channels displayed several equivalent conductance levels, which suggest an oligomeric pore structure. We conclude that the 450,000-dalton polypeptide ryanodine receptor is the Ca-release channel of the sarcoplasmic reticulum and is the target site of ruthenium red and ryanodine.

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15

Arellano, R. O., R. M. Woodward, and R. Miledi. "A monovalent cationic conductance that is blocked by extracellular divalent cations in Xenopus oocytes." Journal of Physiology 484, no. 3 (May 1, 1995): 593–604. http://dx.doi.org/10.1113/jphysiol.1995.sp020689.

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16

Amarillo, Yimy, Edward Zagha, German Mato, Bernardo Rudy, and Marcela S. Nadal. "The interplay of seven subthreshold conductances controls the resting membrane potential and the oscillatory behavior of thalamocortical neurons." Journal of Neurophysiology 112, no. 2 (July 15, 2014): 393–410. http://dx.doi.org/10.1152/jn.00647.2013.

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The signaling properties of thalamocortical (TC) neurons depend on the diversity of ion conductance mechanisms that underlie their rich membrane behavior at subthreshold potentials. Using patch-clamp recordings of TC neurons in brain slices from mice and a realistic conductance-based computational model, we characterized seven subthreshold ion currents of TC neurons and quantified their individual contributions to the total steady-state conductance at levels below tonic firing threshold. We then used the TC neuron model to show that the resting membrane potential results from the interplay of several inward and outward currents over a background provided by the potassium and sodium leak currents. The steady-state conductances of depolarizing Ih (hyperpolarization-activated cationic current), IT (low-threshold calcium current), and INaP (persistent sodium current) move the membrane potential away from the reversal potential of the leak conductances. This depolarization is counteracted in turn by the hyperpolarizing steady-state current of IA (fast transient A-type potassium current) and IKir (inwardly rectifying potassium current). Using the computational model, we have shown that single parameter variations compatible with physiological or pathological modulation promote burst firing periodicity. The balance between three amplifying variables (activation of IT, activation of INaP, and activation of IKir) and three recovering variables (inactivation of IT, activation of IA, and activation of Ih) determines the propensity, or lack thereof, of repetitive burst firing of TC neurons. We also have determined the specific roles that each of these variables have during the intrinsic oscillation.

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Amarillo, Yimy, Angela I. Tissone, Germán Mato, and Marcela S. Nadal. "Inward rectifier potassium current IKir promotes intrinsic pacemaker activity of thalamocortical neurons." Journal of Neurophysiology 119, no. 6 (June 1, 2018): 2358–72. http://dx.doi.org/10.1152/jn.00867.2017.

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Slow repetitive burst firing by hyperpolarized thalamocortical (TC) neurons correlates with global slow rhythms (<4 Hz), which are the physiological oscillations during non-rapid eye movement sleep or pathological oscillations during idiopathic epilepsy. The pacemaker activity of TC neurons depends on the expression of several subthreshold conductances, which are modulated in a behaviorally dependent manner. Here we show that upregulation of the small and neglected inward rectifier potassium current IKir induces repetitive burst firing at slow and delta frequency bands. We demonstrate this in mouse TC neurons in brain slices by manipulating the Kir maximum conductance with dynamic clamp. We also performed a thorough theoretical analysis that explains how the unique properties of IKir enable this current to induce slow periodic bursting in TC neurons. We describe a new ionic mechanism based on the voltage- and time-dependent interaction of IKir and hyperpolarization-activated cationic current Ih that endows TC neurons with the ability to oscillate spontaneously at very low frequencies, even below 0.5 Hz. Bifurcation analysis of conductance-based models of increasing complexity demonstrates that IKir induces bistability of the membrane potential at the same time that it induces sustained oscillations in combination with Ih and increases the robustness of low threshold-activated calcium current IT-mediated oscillations. NEW & NOTEWORTHY The strong inwardly rectifying potassium current IKir of thalamocortical neurons displays a region of negative slope conductance in the current-voltage relationship that generates potassium currents activated by hyperpolarization. Bifurcation analysis shows that IKir induces bistability of the membrane potential; generates sustained subthreshold oscillations by interacting with the hyperpolarization-activated cationic current Ih; and increases the robustness of oscillations mediated by the low threshold-activated calcium current IT. Upregulation of IKir in thalamocortical neurons induces repetitive burst firing at slow and delta frequency bands (<4 Hz).

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Kleine, Teri J., Gerald J. Gleich, and Simon A. Lewis. "Eosinophil peroxidase increases membrane permeability in mammalian urinary bladder epithelium." American Journal of Physiology-Cell Physiology 276, no. 3 (March 1, 1999): C638—C647. http://dx.doi.org/10.1152/ajpcell.1999.276.3.c638.

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Eosinophil peroxidase (EPO), a cationic protein found in eosinophils, has been reported to be cytotoxic independent of its peroxidase activity. This study investigated with electrophysiological methods whether EPO is toxic to mammalian urinary bladder epithelium. Results indicate that EPO, when added to the mucosal solution, increases apical membrane conductance of urinary bladder epithelium only when the apical membrane potential is cell interior negative. The EPO-induced conductance was concentration dependent, with a maximum conductance of 411 μS/cm2 and a Michaelis-Menten constant of 113 nM. The EPO-induced conductance was nonselective for K+ and Cl−. The conductance was partially reversed using voltage but not by removal of EPO from the bulk solution. Mucosal Ca2+reversed the EPO-induced conductance by a mechanism involving reversible block of the conductance. Prolonged exposure (up to 1 h) to EPO was toxic to the urinary bladder epithelium, as indicated by an irreversible increase in transepithelial conductance. These results suggest that EPO is indeed toxic to urinary bladder epithelium via a mechanism that involves an increase in membrane permeability.

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Jones, Leslie Sargent, and Darrell V. Lewis. "A calcium-activated, nonselective cationic conductance in Aplysia silent neurons." Brain Research Bulletin 20, no. 5 (May 1988): 607–9. http://dx.doi.org/10.1016/0361-9230(88)90220-1.

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Wang, Junjie, David George Jackson, and Gerhard Dahl. "Cationic control of Panx1 channel function." American Journal of Physiology-Cell Physiology 315, no. 3 (September 1, 2018): C279—C289. http://dx.doi.org/10.1152/ajpcell.00303.2017.

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The sequence and predicted membrane topology of pannexin1 (Panx1) places it in the family of gap junction proteins. However, rather than forming gap junction channels, Panx1 forms channels in the nonjunctional membrane. Panx1 operates in two distinct open states, depending on the mode of stimulation. The exclusively voltage-gated channel has a small conductance (<100 pS) and is highly selective for the flux of chloride ions. The Panx1 channel activated by various physiological stimuli or by increased concentrations of extracellular potassium ions has a large conductance (~500 pS, however, with multiple, long-lasting subconductance states) and is nonselectively permeable to small molecules, including ATP. To test whether the two open conformations also differ pharmacologically, the effects of di-and trivalent cations on the two Panx1 channel conformations were investigated. The rationale for this venture was that, under certain experimental conditions, ATP release from cells can be inhibited by multivalent cations, yet the literature indicates that the ATP release channel Panx1 is not affected by these ions. Consistent with previous reports, the Panx1 channel was not activated by removal of extracellular Ca2+ and the currents through the voltage-activated channel were not altered by Ca2+, Zn2+, Ba2+, or Gd3+. In contrast, the Panx1 channel activated to the large channel conformation by extracellular K+, osmotic stress, or low oxygen was inhibited by the multivalent cations in a dose-dependent way. Thus, monovalent cations activated the Panx1 channel from the closed state to the “large” conformation, while di- and trivalent cations exclusively inhibited this large channel conformation.

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Bolívar, Juan J., Dagoberto Tapia, Gabina Arenas, Mauricio Castañón-Arreola, Haydee Torres, and Elvira Galarraga. "A hyperpolarization-activated, cyclic nucleotide-gated, (Ih-like) cationic current and HCN gene expression in renal inner medullary collecting duct cells." American Journal of Physiology-Cell Physiology 294, no. 4 (April 2008): C893—C906. http://dx.doi.org/10.1152/ajpcell.00616.2006.

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The cation conductancein primary cultures of rat renal inner medullary collecting duct was studied using perforated-patch and conventional whole cell clamp techniques. Hyperpolarizations beyond −60 mV induced a time-dependent inward nonselective cationic current ( Ivti) that resembles the well-known hyperpolarization-activated, cyclic nucleotide-gated Ih and If currents. Ivti showed a half-maximal activation around −102 mV with a slope factor of 25 mV. It had a higher conductance (but, at its reversal potential, not a higher permeability) for K+ than for Na+ ( gK+/ gNa+ = 1.5), was modulated by cAMP and blocked by external Cd2+ (but not Cs+ or ZD-7288), and potentiated by a high extracellular K+ concentration. We explored the expression of the Ih channel genes (HCN1 to -4) by RT-PCR. The presence of transcripts corresponding to the HCN1, -2, and -4 genes was observed in both the cultured cells and kidney inner medulla. Western blot analysis with HCN2 antibody showed labeling of ∼90- and ∼120-kDa proteins in samples from inner medulla and cultured cells. Immunocytochemical analysis of cell cultures and inner medulla showed the presence of HCN immunoreactivity partially colocalized with the Na+-K+-ATPase at the basolateral membrane of collecting duct cells. This is the first evidence of an Ih-like cationic current and HCN immunoreactivity in either kidney or any other nonexcitable mammalian cells.

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Khanal, Manoj. "Study of Methyl Orange-Cetyltrimethyl Ammonium Bromide Interaction by Conductivity Method in Methanol-Water Mixed Solvent Media." International Journal of Applied Sciences and Biotechnology 5, no. 2 (June 29, 2017): 172–79. http://dx.doi.org/10.3126/ijasbt.v5i2.17622.

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The interaction of an anionic dye (Methyl Orange) with cationic surfactant (Cetyltrimethylammonium Bromide, CTAB) in the series of solvent containing variable compositions of methanol-water mixture (10%, 20%, 30% and 40%) was studied at room temperature (31±2oC). Conductivity measurements were done for the investigation of interaction of dyes. The specific conductance of 6.58x10-5 M to 59.22x10-5M surfactant (CTAB) and these surfactants with 1.008x10-3M dye (MO) mixtures were noted at room temperature. A theoretical model was used to calculate conductance ratio from the data of measured specific conductance values. Values of conductance ratio of CTAB-MO mixtures were found to be all less than 1 which indicated that CTAB-MO dye -surfactant mixture exert significant influence on the degree of interaction.Int. J. Appl. Sci. Biotechnol. Vol 5(2): 172-179

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23

Madrid, Rodolfo, Ricardo Delgado, and Juan Bacigalupo. "Cyclic AMP Cascade Mediates the Inhibitory Odor Response of Isolated Toad Olfactory Receptor Neurons." Journal of Neurophysiology 94, no. 3 (September 2005): 1781–88. http://dx.doi.org/10.1152/jn.01253.2004.

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Odor stimulation may excite or inhibit olfactory receptor neurons (ORNs). It is well established that the excitatory response involves a cyclic AMP (cAMP) transduction mechanism that activates a nonselective cationic cyclic nucleotide-gated (CNG) conductance, accompanied by the activation of a Ca2+-dependent Cl− conductance, both causing a depolarizing receptor potential. In contrast, odor inhibition is attributed to a hyperpolarizing receptor potential. It has been proposed that a Ca2+-dependent K+ (KCa) conductance plays a key role in odor inhibition, both in toad and rat isolated olfactory neurons. The mechanism underlying odor inhibition has remained elusive. We assessed its study using various pharmacological agents and caged compounds for cAMP, Ca2+, and inositol 1,4,5-triphosphate (InsP3) on isolated toad ORNs. The odor-triggered KCa current was reduced on exposing the cell either to the CNG channel blocker LY83583 (20 μM) or to the adenylyl cyclase inhibitor SQ22536 (100 μM). Photorelease of caged Ca2+ activated a Cl− current sensitive to niflumic acid (10 μM) and a K+ current blockable by charybdotoxin (20 nM) and iberiotoxin (20 nM). In contrast, photoreleased Ca2+ had no effect on cells missing their cilia, indicating that these conductances are confined to the cilia. Photorelease of cAMP induced a charybdotoxin-sensitive K+ current in intact ORNs. Photorelease of InsP3 did not increase the membrane conductance of olfactory neurons, arguing against a direct role of InsP3 in chemotransduction. We conclude that a cAMP cascade mediates the activation of the ciliary Ca2+-dependent K+ current and that the Ca2+ ions that activate the inhibitory current enter the cilia through CNG channels.

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24

Achard, J. M., J. K. Bubien, D. J. Benos, and D. G. Warnock. "Stretch modulates amiloride sensitivity and cation selectivity of sodium channels in human B lymphocytes." American Journal of Physiology-Cell Physiology 270, no. 1 (January 1, 1996): C224—C234. http://dx.doi.org/10.1152/ajpcell.1996.270.1.c224.

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Stretch-mediated regulation of amiloride-sensitive Na+ channels was examined in Epstein-Barr virus-transformed human B lymphocytes. Cation conductances were measured using whole cell patch-clamp techniques. Stretch activation, induced by increasing the hydrostatic pressure of the bath solution, immediately and reversibly increased both inward and outward ionic conductances once a threshold of 2-5 mmH2O was reached. Ionic substitutions confirmed that stretch enhanced membrane conductivity for both Na+ and K+. Amiloride (2 microM) completely prevented the response to elevated hydrostatic pressure; however, when amiloride was applied after stretch-induced activation, the sensitivity to amiloride was dramatically decreased (inhibitor concentration that reduces whole cell current by 50% of approximately 20 microM). Evidence that the currents induced by stretch were mediated by Na+ channels was provided by the lack of response to stretch in lymphocytes from patients with Liddle's syndrome, which is caused by expression of a truncated mutant of the beta-subunit of the amiloride-sensitive Na+ channel. Pretreatment with colchicine (0.5 mM, 30 min) prevented stretch-induced activation, which shows evidence of the involvement of the cytoskeleton. These data indicate that stretch regulates the conductance of amiloride-sensitive Na+ channels in immortalized human B lymphocytes and also alters its cationic selectivity and its sensitivity to amiloride.

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25

Goraczniak, R. M., T. Duda, A. Sitaramayya, and R. K. Sharma. "Structural and functional characterization of the rod outer segment membrane guanylate cyclase." Biochemical Journal 302, no. 2 (September 1, 1994): 455–61. http://dx.doi.org/10.1042/bj3020455.

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In the vertebrate photoreceptor cell, rod outer segment (ROS) is the site of visual signal-transduction process, and a pivotal molecule that regulates this process is cyclic GMP. Cyclic GMP controls the cationic conductance into the ROS, and light causes a decrease in the conductance by activating hydrolysis of the cyclic nucleotide. The identity of the granylate cyclase (ROS-GC) that synthesizes this pool of cyclic GMP is unknown. We now report the cloning, expression and functional characterization of a DNA from bovine retina that encodes ROS-GC.

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26

Swandulla, D. "Cationic membrane conductances induced by intracellularly elevated cAMP and Ca2+: measurements with ion-selective microelectrodes." Canadian Journal of Physiology and Pharmacology 65, no. 5 (May 1, 1987): 898–903. http://dx.doi.org/10.1139/y87-145.

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Adenosine 3′,5′-cyclic monophosphate (cAMP) and CaCl2 were injected by a fast and quantitative pressure injection technique into voltage-clamped, identified Helix neurons. Intracellular elevation of cAMP as well as of Ca2+ activated an inward current (IcAMP and IN). To identify the ionic fluxes during IcAMP and IN changes in [Na+]i, [K+]o, [H+]i, and [Cl−]i were measured with ion-selective microelectrodes (ISMs). Near resting potential, Na+ was the main carrier of IcAMP. K+, and less effectively Ca2+, could substitute for Na+ in carrying IcAMp. H+ and Cl− were excluded as current carriers for IcAMP by means of ISMs. Simultaneous to this action, cAMP decreased a K+ conductance. This decrease was associated with a reduction of the K+ efflux activated by long-lasting depolarizing voltage steps, as directly measured with ISMs located near the external membrane surface. The nearly compensatory increase and decrease of two membrane conductances in the same neuron left the cell input resistance unchanged despite the considerable depolarizing action of intracellularly elevated cAMP. IN was also of nonspecific nature. However, our findings indicate less selectivity for the Ca2+-activated nonspecific channels. Large cations such as choline, TEA, and Tris passed nearly as well as Na+ through the channels. Measurements with ISMs showed that [H+]i and [Cl−]i were unchanged during IN. IN was largest in bursting pacemaker neurons compared with other cells of similar size. It was found to be essential for the burst production in these cells. IcAMP, on the other hand, might be involved in the presynaptic facilitatory action of cAMP, which as yet was attributed solely to a reduction of a K+ conductance.

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27

Fedorenko, E. A., O. V. Semenova, and S. M. Marchenko. "Properties of Large-Conductance Cationic Channels in the Neuronal Nuclear Envelope." Neurophysiology 43, no. 3 (November 2011): 192–94. http://dx.doi.org/10.1007/s11062-011-9202-8.

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28

Berg, Jamie R., Christian M. Spilker, and Simon A. Lewis. "Modulation of polymyxin B effects on mammalian urinary bladder." American Journal of Physiology-Renal Physiology 275, no. 2 (August 1, 1998): F204—F215. http://dx.doi.org/10.1152/ajprenal.1998.275.2.f204.

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This report demonstrates that Ca2+, Mg2+, and protons alter the ability of polymyxin B (PX, a cationic antibiotic used clinically as a bactericidal agent) to increase the apical membrane conductance of the rabbit urinary bladder. Using electrophysiological methods, we determine that these alterations occur by two mechanisms. First, they blocked the PX-induced conductance in a rapid and reversible manner; second, they competed with PX for a membrane binding site. In addition, Ca2+(but not Mg2+or protons) altered the rate at which the induced conductance could be reversed. When solution pH was greater than 8.8, PX was not able to induce a conductance. This ability of high pH to inhibit the action of PX was due to a decrease in the number of positive charges on PX. Further studies demonstrated that for maximal activity, PX required its fatty acid tail. These data were used to develop a model describing the mechanism by which PX can induce a conductance in the apical membrane of the rabbit urinary bladder.

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Bera, Achinta, Ajay Mandal, Keka Ojha, and T. Kumar. "Water Solubilization Capacity and Conductance Behaviors of Anionic and Cationic Microemulsion Systems." Journal of Chemical & Engineering Data 56, no. 12 (December 8, 2011): 4422–29. http://dx.doi.org/10.1021/je200291v.

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30

Wu, Tony, and Hung-Li Wang. "CCK-8 excites substantia nigra dopaminergic neurons by increasing a cationic conductance." Neuroscience Letters 170, no. 2 (April 1994): 229–32. http://dx.doi.org/10.1016/0304-3940(94)90325-5.

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31

Schweitzer, Paul, Samuel G. Madamba, and George R. Siggins. "Somatostatin Increases a Voltage-Insensitive K+ Conductance in Rat CA1 Hippocampal Neurons." Journal of Neurophysiology 79, no. 3 (March 1, 1998): 1230–38. http://dx.doi.org/10.1152/jn.1998.79.3.1230.

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Schweitzer, Paul, Samuel G. Madamba, and George R. Siggins. Somatostatin increases a voltage-insensitive K+ conductance in rat CA1 hippocampal neurons. J. Neurophysiol. 79: 1230–1238, 1998. Somatostatin (SST) is a neuropeptide involved in several central processes. In hippocampus, SST hyperpolarizes CA1 pyramidal neurons and augments the K+ M current ( I M). However, the limited involvement of I M at resting potential in these cells suggests that the peptide also may modulate another channel to hyperpolarize hippocampal pyramidal neurons (HPNs). We studied the effect of SST on noninactivating conductances of rat CA1 HPNs in a slice preparation. Using MK886, a specific inhibitor of the enzymatic pathway that leads to the augmentation of I M by SST, we have uncovered and characterized a second conductance activated by the peptide. SST did not affect I M when applied with MK886 or the amplitudes of the slow Ca2+-dependent K+ afterhyperpolarization-current and the cationic Q current but still caused an outward current, indicating that SST acts upon another conductance. In the presence of MK886, SST elicited an outward current that reversed around −100 mV and that displayed a linear current-voltage relationship. Reversal potentials obtained in different external K+ concentrations are consistent with a conductance carried solely by K+ ions. The slope of the current-voltage relationship increased proportionately with the extracellular K+ concentration and remained linear. This suggests that SST opens a voltage-insensitive leak current ( I K(L)) in HPNs not an inwardly rectifying K+ current as reported in other neuron types. A low concentration of extracellular Ba2+ (150 μM) only slightly decreased the SST-induced effect in a voltage-independent manner, whereas a high concentration of Ba2+ (2 mM) completely blocked it. Extracellular Cs+ (2 mM) did not affect the outward SST current but inhibited the inward component. We conclude that SST inhibits HPNs by activating two different K+ conductances: the voltage-insensitive I K(L) and the voltage-dependent I M. The hyperpolarizing effect of SST at resting membrane potential appears to be mainly carried by I K(L), whereas I M dominates at slightly depolarized potentials.

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32

Hamilton, K. L., and D. C. Eaton. "Single-channel recordings from amiloride-sensitive epithelial sodium channel." American Journal of Physiology-Cell Physiology 249, no. 3 (September 1, 1985): C200—C207. http://dx.doi.org/10.1152/ajpcell.1985.249.3.c200.

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We report here the first evidence in intact epithelial cells of unit conductance events from an amiloride-sensitive Na+ channel. The events were observed when patch-clamp recordings were made from the apical surface of cultured epithelial kidney cells (A6). The channel characteristics are as follows. Single-channel conductance ranged between 7 and 10 pS (mean = 8.4 +/- 1.3), the current-voltage (I-V) relationship displayed little if any nonlinearity over a range of +/- 80 mV (with respect to the patch pipette), and the channel Na+/K+ selectivity was approximately 3-4:1. Amiloride, a cationic blocker of the channel, reduced channel mean open time and increased channel mean closed time as the voltage of the cell interior was made more negative. Amiloride induced channel flickering at increased negative potentials (intracellular potential with respect to the patch) but did not alter the single-channel conductance or the I-V relationship from that observed in control patches.

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Li, Allen H., Hwa-Min Hwang, Peter P. Tan, Tony Wu, and Hung-Li Wang. "Neurotensin Excites Periaqueductal Gray Neurons Projecting to the Rostral Ventromedial Medulla." Journal of Neurophysiology 85, no. 4 (April 1, 2001): 1479–88. http://dx.doi.org/10.1152/jn.2001.85.4.1479.

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Microinjection of neurotensin into the midbrain periaqueductal gray (PAG) produces a potent and naloxone-insensitive analgesic effect. To test the hypothesis that neurotensin induces the analgesic effect by activating the PAG-rostral ventromedial medulla (RVM) descending antinociceptive pathway, PAG neurons that project to RVM (PAG-RVM) were identified by microinjecting DiIC18, a retrograde tracing dye, into the rat RVM. Subsequently, fluorescently labeled PAG-RVM projection neurons were acutely dissociated and selected for whole cell patch-clamp recordings. During current-clamp recordings, neurotensin depolarized retrogradely labeled PAG-RVM neurons and evoked action potentials. Voltage-clamp recordings indicated that neurotensin excited PAG-RVM neurons by opening the voltage-insensitive and nonselective cation channels. Both SR 48692, a selective NTR-1 antagonist, and SR 142948A, a nonselective antagonist of NTR-1 and NTR-2, failed to prevent neurotensin from exciting PAG-RVM neurons. Neurotensin failed to evoke cationic currents after internally perfusing PAG-RVM projection neurons with GDP-β-S or anti-Gα q/11 antiserum. Cellular Ca2+ fluorescence measurement using fura-2 indicated that neurotensin rapidly induced Ca2+ release from intracellular stores of PAG-RVM neurons. Neurotensin-evoked cationic currents were blocked by heparin, an IP3 receptor antagonist, and 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid (BAPTA), a fast chelator of Ca2+. These results suggest that by activating a novel subtype of neurotensin receptors, neurotensin depolarizes and excites PAG-RVM projection neurons through enhancing Ca2+-dependent nonselective cationic conductance. The coupling mechanism via Gα q/11 proteins is likely to involve the production of IP3, and subsequent IP3-evoked Ca2+ release leads to the opening of nonselective cation channels.

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34

Yang, Bo, Martin Goulet, Richard Boismenu, and Alastair V. Ferguson. "Secretin depolarizes nucleus tractus solitarius neurons through activation of a nonselective cationic conductance." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 286, no. 5 (May 2004): R927—R934. http://dx.doi.org/10.1152/ajpregu.00600.2003.

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The recent suggestion that secretin may be useful in treating autism and schizophrenia has begun to focus attention on the mechanisms underlying this gut-brain peptide's actions in the central nervous system (CNS). In vitro autoradiographic localization of 125I-secretin binding sites in rat brain shows the highest binding density in the nucleus tractus solitarius (NTS). Recent evidence suggests that intravenous infusion of secretin causes fos activation in NTS, a relay station playing important roles in the central regulation of autonomic functions. In this study, whole cell patch-clamp recordings were obtained from 127 NTS neurons in rat medullary slices. The mean resting membrane potential of these neurons was -54.7 ± 0.3 mV, the mean input resistance was 3.7 ± 0.2 GΩ, and the action potential amplitude of these neurons was always >70 mV. Current-clamp studies showed that bath application of secretin depolarized the majority (80.8%; 42/52) of NTS neurons tested, whereas the remaining cells were either unaffected (17.3%; 9/52) or hyperpolarized (1.9%; 1/52). These depolarizing effects were maintained in the presence of 5 μM TTX and found to be concentration dependent from 10-12 to 10-7 M. Using voltage-clamp techniques, we also identified modulatory actions of secretin on specific ion channels. Our results demonstrate that while secretin is without effect on net whole cell potassium currents, it activates a nonselective cationic conductance (NSCC). These results show that NTS neurons are activated by secretin as a consequence of activation of a NSCC and support the emerging view that secretin can act as a neuropeptide within the CNS.

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35

Hlavac, Nora, Fernanda Guilhaume-Corrêa, and Pamela J. VandeVord. "Mechano-stimulation initiated by extracellular adhesion and cationic conductance pathways influence astrocyte activation." Neuroscience Letters 739 (November 2020): 135405. http://dx.doi.org/10.1016/j.neulet.2020.135405.

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36

Shan, Yuping, Namuna Panday, Yong Myoung, Megan Twomey, Xuewen Wang, Wenzhi Li, Emrah Celik, et al. "Scanning Ion Conductance Microscopic Study for Cellular Uptake of Cationic Conjugated Polymer Nanoparticles." Macromolecular Bioscience 16, no. 4 (January 12, 2016): 599–607. http://dx.doi.org/10.1002/mabi.201500320.

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37

Thieffry, M., J. F. Chich, D. Goldschmidt, and J. P. Henry. "Incorporation in lipid bilayers of a large conductance cationic channel from mitochondrial membranes." EMBO Journal 7, no. 5 (May 1988): 1449–54. http://dx.doi.org/10.1002/j.1460-2075.1988.tb02962.x.

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Tissone, Angela Isabel, Varinia Beatriz Vidal, Marcela Silvia Nadal, German Mato, and Yimy Amarillo. "Differential contribution of the subthreshold operating currents IT, Ih, and IKir to the resonance of thalamocortical neurons." Journal of Neurophysiology 126, no. 2 (August 1, 2021): 561–74. http://dx.doi.org/10.1152/jn.00147.2021.

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Our study expands the repertoire of ionic mechanisms known to be involved in the generation and control of resonance and provides the first experimental proof of previous theoretical predictions on resonance amplification mediated by regenerative hyperpolarizing currents. In thalamocortical neurons, we confirmed that the calcium current IT generates resonance, determined that the large steady conductance of the cationic current Ih curtails resonance, and demonstrated that the inward rectifier potassium current IKir amplifies resonance.

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39

Santa Cruz, Ana, Gülistan Meşe, Laima Valiuniene, Peter R. Brink, Thomas W. White, and Virginijus Valiunas. "Altered conductance and permeability of Cx40 mutations associated with atrial fibrillation." Journal of General Physiology 146, no. 5 (October 26, 2015): 387–98. http://dx.doi.org/10.1085/jgp.201511475.

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Gap junctions ensure the rapid propagation of the action potential throughout the myocardium. Three mutant forms of connexin40 (Cx40; A96S, M163V, and G38D), the primary component of the atrial gap junction channel, are associated with atrial fibrillation and retain the ability to form functional channels. We determined the biophysical properties of these mutant gap junctions in transiently transfected HeLa and N2A cells. All three mutants showed macroscopic junctional conductances over the range of 0.5 to 40 nS, and voltage dependences comparable to those of wild-type (WT) Cx40. However, the unitary conductance of G38D channels was ∼1.6-fold higher than that of WT Cx40 channels (∼220 vs. ∼135 pS), whereas the unitary conductances of the A96S and M163V mutants were similar to that of WT Cx40. Furthermore, the M163V and G38D channels exhibited approximately two- and approximately fivefold higher permeability to the anionic dye Lucifer yellow (LY) relative to K+ (LY/K+) compared with that of WT Cx40, whereas A96S LY transfer was similar to that of WT (G38D > M163V > A96S ≈ Cx40WT). In contrast, G38D channels were almost impermeable to cationic ethidium bromide (EtBr), suggesting that G38D alters channel selectivity. Conversely, A96S and M163V channels showed enhanced EtBr permeability relative to WT Cx40, with the following permeability order: M163V > A96S > Cx40WT > G38D. Altered conductive and permeability properties of mutant channels suggest an essential role for Cx40-mediated biochemical and electrical coupling in cardiac tissues. The altered properties of the three single-base substitution mutants may play a role in mechanisms of reentry arrhythmias.

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Lima, Geovani S. de, Hans R. Gheyi, Reginaldo G. Nobre, Lauriane A. dos A. Soares, Leandro de P. Souza, Francisco Wesley A. Pinheiro, Adaan S. Dias, and Sabrina G. de Oliveira. "Physiological Indices and Growth of Castor Bean Irrigated With Waters of Different Cationic Nature." Journal of Agricultural Science 10, no. 10 (September 15, 2018): 405. http://dx.doi.org/10.5539/jas.v10n10p405.

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It was proposed, in the present study, to evaluate the gas exchange and the growth of the castor bean cv. BRS Energia due to the isolated or mixed cationic nature of irrigation water. The study was conducted in drainage lysimeters under greenhouse conditions, using an Eutrophic Greyish Argissolo with a sandy-loam texture in the municipality of Campina Grande, Brazil. A randomized block design was used with six cationic composition of irrigation water (S1-control, S2-Na+, S3-Ca2+, S4-Na++Ca2+, S5-K+ and S6-Na++Ca2++Mg2+ with four replicates, each composed of five plants. The plants under the control treatment were submitted to irrigation with low salinity water (ECw = 0.6 dS m-1) and the remaining treatments were irrigated with ECw of 4.5 dS m-1 prepared with salts of different cations in chloride form. The gas exchanges and the growth of the castor bean cv. BRS Energy were determined at 100 days after sowing. The gas exchanges and the growth of the castor cv. BRS Energy were more sensitive to the variation in the electrical conductivity of the water compared to the cationic nature of the water, being the least deleterious effect observed in the plants irrigated with potassic water. The plants irrigated with water of potassium composition obtained the highest values for stomatal conductance, transpiration and rate of assimilation of CO2; at 100 days after sowing; the castor bean cv. BRS Energia showed sensitivity to the presence of sodium and calcium salts in irrigation water.

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Klink, R., and A. Alonso. "Ionic mechanisms for the subthreshold oscillations and differential electroresponsiveness of medial entorhinal cortex layer II neurons." Journal of Neurophysiology 70, no. 1 (July 1, 1993): 144–57. http://dx.doi.org/10.1152/jn.1993.70.1.144.

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1. Layer II of the medial entorhinal cortex is composed of two electrophysiologically and morphologically distinct types of projection neurons: stellate cells (SCs), which are distinguished by rhythmic subthreshold oscillatory activity, and non-SCs. The ionic mechanisms underlying their differential electroresponsiveness, particularly in the subthreshold range of membrane potentials, were investigated in an "in vitro" slice preparation. 2. In both SCs and non-SCs, the apparent membrane input resistance was markedly voltage dependent, respectively decreasing or increasing at hyperpolarized or subthreshold depolarized potential levels. Thus the neurons displayed inward rectification in the hyperpolarizing and depolarizing range. 3. In the depolarizing range, inward rectification was blocked by tetrodotoxin (TTX, 1 microM) in both types of neurons and thus shown to depend on the presence of a persistent low-threshold Na+ conductance (gNap). However, in the presence of TTX, pronounced outward rectification became manifest in the subthreshold depolarizing range of membrane potentials (positive to -60 mV) in the SCs but not in the non-SCs. 4. The rhythmic subthreshold membrane potential oscillations that were present only in the SCs were abolished by TTX and not by Ca2+ conductance block with Cd2+ or Co2+. Subthreshold oscillations thus rely on the activation of voltage-gated Na+, and not Ca2+, conductances. The Ca2+ conductance block also had no effect on the subthreshold outward rectification. 5. Prominent time-dependent inward rectification in the hyperpolarizing range in the SCs persisted after Na(+)- and Ca2+ conductance block. This rectification was not affected by Ba2+ (1 mM), but was blocked by Cs+ (1-4 mM). Therefore, it is most probably generated by a hyperpolarization-activated cationic current (Q-like current). However, the Q-like current appears to play no major role in the generation of subthreshold rhythmic membrane potential oscillations, because these persisted in the presence of Cs+. 6. On the other hand, in the SCs, the fast, sustained, outward rectification that strongly developed (after Na+ conductance block) at the oscillatory voltage level was not affected by Cs+ but was blocked by Ba2+ (1 mM). Barium was also effective in blocking the subthreshold membrane potential oscillations. 7. In the non-SCs, which do not generate subthreshold rhythmic membrane potential oscillations or manifest subthreshold outward rectification in TTX, Ca2+ conductance block abolished spike repolarization and caused the development of long-lasting Na(+)-dependent plateau potentials at a high suprathreshold voltage level. At this level, where prominent delayed rectification is present, the Na+ plateaus sustained rhythmic membrane potential oscillations.(ABSTRACT TRUNCATED AT 400 WORDS)

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Yang, Bo, and Alastair V. Ferguson. "Orexin-A Depolarizes Nucleus Tractus Solitarius Neurons Through Effects on Nonselective Cationic and K+ Conductances." Journal of Neurophysiology 89, no. 4 (April 1, 2003): 2167–75. http://dx.doi.org/10.1152/jn.01088.2002.

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The nucleus tractus solitarius (NTS) plays central roles in a number of autonomic functions including cardiovascular control. Orexin (ORX)-A is a 33-amino-acid peptide implicated in the central regulation of energy metabolism, sleep, and the cardiovascular system. Studies demonstrate the presence of ORX-immunoreactive axons and both OX1R (orexin receptor) and OX2R mRNA within NTS. In this study, whole cell patch-clamp recordings were obtained from NTS neurons in rat medullary slices. Current-clamp studies showed that bath application of various concentrations of ORX-A depolarized 90.7% (78 of 86) of neurons tested while the remaining cells were either unaffected or showed small hyperpolarizations in response to peptide administration. Depolarizing effects were maintained in the presence of 5 μM TTX, and were concentration dependent. Using voltage-clamp techniques, we also identified modulatory actions of ORX-A on specific ion channels. Our results demonstrate that not only does ORX-A inhibit a specific potassium conductance (the sustained K+ current) in NTS neurons, but it also activates a nonselective cationic conductance (NSCC). These data suggest that ORX-A effects on central cardiovascular control may result from direct actions on NTS neurons and also highlight the ability of this peptide to influence neuronal excitability as a consequence of concurrent modulation of multiple ion channels.

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Balleza, Daniel, Froylán Gómez-Lagunas, Federico Sánchez, and Carmen Quinto. "A high conductance cationic channel from Phaseolus vulgaris roots incorporated into planar lipid bilayers." Archives of Biochemistry and Biophysics 438, no. 1 (June 2005): 88–92. http://dx.doi.org/10.1016/j.abb.2005.04.007.

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44

Van Driessche, W., and D. Erlij. "Activation of K+ conductance in basolateral membrane of toad urinary bladder by oxytocin and cAMP." American Journal of Physiology-Cell Physiology 254, no. 6 (June 1, 1988): C816—C821. http://dx.doi.org/10.1152/ajpcell.1988.254.6.c816.

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We incubated toad urinary bladders with Na+-free, isotonic K+ solutions on the apical side and increased the cationic conductance of the apical membrane with nystatin (150 U/ml). Under these conditions, the short-circuit current is mostly carried by K+ flowing from mucosa to serosa. Impedance measurements showed that in nystatin-treated preparations, the electrical behavior of the tissue is dominated by the basolateral membrane properties. Oxytocin (0.1 U/ml) produced an increase of the current and the conductance of the basolateral membrane. Both the resting and the oxytocin-stimulated current were rapidly and reversibly blocked by serosal Ba2+. Addition of the adenosine 3',5'-cyclic monophosphate (cAMP) analogue [8-(4-chloropheylthio)-cAMP] to the basolateral solution mimicked the effects of oxytocin. These results show that oxytocin and cAMP stimulate a potassium conductance in the basolateral membrane and that the stimulation is not related to an increase in sodium entry through the apical membrane. Addition of ouabain (10(-3) M) to the serosal solution did not modify the stimulation by oxytocin, indicating that the activated pathway is not linked to the rate of turnover of the Na+ pump.

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Herness, M. Scott, and Xiao-Dong Sun. "Characterization of Chloride Currents and Their Noradrenergic Modulation in Rat Taste Receptor Cells." Journal of Neurophysiology 82, no. 1 (July 1, 1999): 260–71. http://dx.doi.org/10.1152/jn.1999.82.1.260.

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Taste receptor cells contain a heterogeneous array of voltage-dependent ion conductances that are essential components for the transduction of gustatory stimuli. Although mechanistic roles have been proposed for several cationic conductances, the understanding of anionic currents is rudimentary. This study characterizes biophysical and pharmacological properties of chloride currents in rat posterior taste cells using whole cell patch-clamp recording technique. Taste cells express a heterogeneous array of chloride currents that displayed strong outward rectification, contained both calcium–dependent and calcium–independent components, and achieved a maximal conductance of almost 1 nS. Reversal potentials altered predictably with changes in chloride concentration. Currents were sensitive to inhibition by the chloride channel pharmacological agents DIDS, SITS, and niflumic acid but were insensitive to 9-AC. Adrenergic enhancement of chloride currents, present in other cell types, was tested on taste cells with the β-adrenergic agonist isoproterenol (ISP). ISP enhanced the outwardly rectifying portion of the chloride current. This enhancement was calcium dependent and was blocked by the β-adrenergic antagonist propranolol. Collectively these observations suggest that chloride currents may participate not only in usually ascribed functions such as stabilization of the membrane potential and volume regulation but additionally play active modulatory roles in the transduction of gustatory stimuli.

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Navarro, Franz E. C., José A. Santos Júnior, Juliana B. Martins, Ruana I. F. Cruz, Manassés M. da Silva, and Salomão de S. Medeiros. "Physiological aspects and production of coriander using nutrient solutions prepared in different brackish waters." Revista Brasileira de Engenharia Agrícola e Ambiental 26, no. 11 (November 2022): 831–39. http://dx.doi.org/10.1590/1807-1929/agriambi.v26n11p831-839.

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ABSTRACT The analysis of chlorophyll fluorescence is one of many ways to quantify the salt damage to photosynthetic performance and crop production. Thus, the present study aimed to evaluate the photochemical efficiency and production of coriander, cultivar ‘Verdão’, as a function of the electrical conductivity levels of the nutrient solution and the cationic nature. The experimental design was in randomized blocks, in a 4 × 3 factorial scheme, with four replicates. The treatments consisted of four electrical conductivities of the nutrient solutions (ECns = 1.6, 3.2, 4.8, and 6.4 dS m-1) and three kinds of water of different cationic natures (Na+; Ca2+; Mg2+), which were prepared with the dissolution of different salts - NaCl, CaCl2.2H2O, and MgCl2.6H2O in supply water (ECw = 0.12 dS m-1), that is, three predominant cationic natures. The study was carried out in a greenhouse between November and December 2019 at the Fertigation and Salinity Laboratory of the Agricultural Engineering Department of the Universidade Federal Rural de Pernambuco. It was found that the increase in the electrical conductivity of the nutrient solution affected reaction centers, photochemical activity, and carboxylation efficiency and resulted in reductions in stomatal conductance, CO2 assimilation rate, and therefore, in the biomass production of coriander. Different cationic prevalence in water causes differences in the intensity of salt damage, especially with increasing concentration.

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Navarro, Franz E. C., Ivis A. C. e. Silva, José A. Santos Júnior, Tarcísio F. de Oliveira, Gerônimo F. da Silva, and Ênio F. de F. e. Silva. "Hydroponic coriander grown under nutritional solutions prepared with brackish water of different cation prevalence." Revista Brasileira de Engenharia Agrícola e Ambiental 27, no. 9 (September 2023): 736–45. http://dx.doi.org/10.1590/1807-1929/agriambi.v27n9p736-745.

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ABSTRACT The use of brackish water for preparation of nutrient solutions has several impacts on crop performance, depending on the water concentration and cation prevalence. Therefore, this study was conducted to evaluate production and water relations of coriander grown on nutrient solutions prepared with brackish waters with different cationic natures under hydroponic conditions. A randomized block experimental design with four replicates was used, in a 4 × 3 factorial arrangement. The treatments consisted of four electrical conductivities of the nutrient solution (1.6, 3.2, 4.8, and 6.4 dS m-1) which were prepared in waters with different salts (NaCl, CaCl2.2H2O, and MgCl2.6H2O). Salinity negatively affected the production and water relations of coriander grown in hydroponic system; plants grown on nutritive solutions with predominance of Na+ had higher total dry weight and shoot dry weights, as well as higher stomatal conductance. The largest leaf area was found when using the nutrient solution with predominance of Mg2+.

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Fesenko, Evgeniy E., Stanislav S. Kolesnikov, and Arkadiy L. Lyubarsky. "Induction by cyclic GMP of cationic conductance in plasma membrane of retinal rod outer segment." Nature 313, no. 6000 (January 1985): 310–13. http://dx.doi.org/10.1038/313310a0.

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Schwegler, Johann S., and Stefan Silbernagl. "Sodium Conductance in Cultured Proximal Tubule Cells (OK) Is Inhibited by Extracellular Cationic Amino Acids." Cellular Physiology and Biochemistry 2, no. 2 (1992): 124–32. http://dx.doi.org/10.1159/000154632.

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Wu, Tony, and Hung-Li Wang. "Gαq/11 Mediates Cholecystokinin Activation of the Cationic Conductance in Rat Substantia Nigra Dopaminergic Neurons." Journal of Neurochemistry 66, no. 3 (November 23, 2002): 1060–66. http://dx.doi.org/10.1046/j.1471-4159.1996.66031060.x.

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Journal articles on the topic 'Cationic conductance'

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