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1

Lai, Xiao-Gang, Jun Yang, Shi-Sheng Zhou, Jun Zhu, Gui-Rong Li, and Tak-Ming Wong. "Involvement of anion channel(s) in the modulation of the transient outward K+ channel in rat ventricular myocytes." American Journal of Physiology-Cell Physiology 287, no. 1 (2004): C163—C170. http://dx.doi.org/10.1152/ajpcell.00297.2003.

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The cardiac Ca2+-independent transient outward K+ current ( Ito), a major repolarizing ionic current, is markedly affected by Cl− substitution and anion channel blockers. We reexplored the mechanism of the action of anions on Ito by using whole cell patch-clamp in single isolated rat cardiac ventricular myocytes. The transient outward current was sensitive to blockade by 4-aminopyridine (4-AP) and was abolished by Cs+ substitution for intracellular K+. Replacement of most of the extracellular Cl− with less permeant anions, aspartate (Asp−) and glutamate (Glu−), markedly suppressed the current.
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2

De Jesús-Pérez, José J., Alejandra Castro-Chong, Ru-Chi Shieh, Carmen Y. Hernández-Carballo, José A. De Santiago-Castillo, and Jorge Arreola. "Gating the glutamate gate of CLC-2 chloride channel by pore occupancy." Journal of General Physiology 147, no. 1 (2015): 25–37. http://dx.doi.org/10.1085/jgp.201511424.

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CLC-2 channels are dimeric double-barreled chloride channels that open in response to hyperpolarization. Hyperpolarization activates protopore gates that independently regulate the permeability of the pore in each subunit and the common gate that affects the permeability through both pores. CLC-2 channels lack classic transmembrane voltage–sensing domains; instead, their protopore gates (residing within the pore and each formed by the side chain of a glutamate residue) open under repulsion by permeant intracellular anions or protonation by extracellular H+. Here, we show that voltage-dependent
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3

Franciolini, F., and W. Nonner. "Anion and cation permeability of a chloride channel in rat hippocampal neurons." Journal of General Physiology 90, no. 4 (1987): 453–78. http://dx.doi.org/10.1085/jgp.90.4.453.

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The ionic permeability of a voltage-dependent Cl channel of rat hippocampal neurons was studied with the patch-clamp method. The unitary conductance of this channel was approximately 30 pS in symmetrical 150 mM NaCl saline. Reversal potentials interpreted in terms of the Goldman-Hodgkin-Katz voltage equation indicate a Cl:Na permeability ratio of approximately 5:1 for conditions where there is a salt gradient. Many anions are permeant; permeability generally follows a lyotropic sequence. Permeant cations include Li, Na, K, and Cs. The unitary conductance does not saturate for NaCl concentratio
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4

Grover, A. K., A. P. Singh, P. K. Rangachari, and P. Nicholls. "Ion movements in membrane vesicles: a new fluorescence method and application to smooth muscle." American Journal of Physiology-Cell Physiology 248, no. 3 (1985): C372—C378. http://dx.doi.org/10.1152/ajpcell.1985.248.3.c372.

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A method is described for studying ion permeabilities of membrane vesicles based on the principle that when membrane permeability to H+ is very high, the H+ movement is determined by the membrane potential generated by the H+ movement. The rate of H+ movement under these conditions thus gives a measure of the rate of dissipation of this membrane potential by comovement of anions or countermovement of cations present. Thus, by studying the H+ efflux using an impermeant cation and different anions, the membrane permeability to the anions can be assessed. Similarly, the use of an impermeant anion
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5

Linsdell, Paul, and John W. Hanrahan. "Adenosine Triphosphate–dependent Asymmetry of Anion Permeation in the Cystic Fibrosis Transmembrane Conductance Regulator Chloride Channel." Journal of General Physiology 111, no. 4 (1998): 601–14. http://dx.doi.org/10.1085/jgp.111.4.601.

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The cystic fibrosis transmembrane conductance regulator (CFTR) forms a tightly regulated channel that mediates the passive diffusion of Cl− ions. Here we show, using macroscopic current recording from excised membrane patches, that CFTR also shows significant, but highly asymmetrical, permeability to a broad range of large organic anions. Thus, all large organic anions tested were permeant when present in the intracellular solution under biionic conditions (PX/PCl = 0.048–0.25), whereas most were not measurably permeant when present in the extracellular solution. This asymmetry was not observe
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6

DAWSON, DAVID C., STEPHEN S. SMITH, and MONIQUE K. MANSOURA. "CFTR: Mechanism of Anion Conduction." Physiological Reviews 79, no. 1 (1999): S47—S75. http://dx.doi.org/10.1152/physrev.1999.79.1.s47.

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Dawson, David C., Stephen S. Smith, and Monique K. Mansoura. CFTR: Mechanism of Anion Conduction. Physiol. Rev. 79, Suppl.: S47–S75, 1999. — The purpose of this review is to collect together the results of recent investigations of anion conductance by the cystic fibrosis transmembrane conductance regulator along with some of the basic background that is a prerequisite for developing some physical picture of the conduction process. The review begins with an introduction to the concepts of permeability and conductance and the Nernst-Planck and rate theory models that are used to interpret these
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7

Linsdell, P., and J. W. Hanrahan. "Flickery block of single CFTR chloride channels by intracellular anions and osmolytes." American Journal of Physiology-Cell Physiology 271, no. 2 (1996): C628—C634. http://dx.doi.org/10.1152/ajpcell.1996.271.2.c628.

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Cystic fibrosis transmembrane conductance regulator (CFTR) is a phosphorylation- and nucleotide-dependent chloride channel. Single CFTR currents recorded on cell show slight outward rectification, which has previously been suggested to be due to an asymmetrical chloride ion gradient or to a specific interaction between permeant intracellular anions and the channel. Using a single-channel recording from Chinese hamster ovary cells stably expressing CFTR, we have found that both the sparingly permeant anion glutamate and the impermeant anion gluconate cause a rapid, voltage-dependent block of CF
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8

Qu, Zhiqiang, and H. Criss Hartzell. "Anion Permeation in Ca2+-Activated Cl− Channels." Journal of General Physiology 116, no. 6 (2000): 825–44. http://dx.doi.org/10.1085/jgp.116.6.825.

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Ca2+-activated Cl channels (ClCaCs) are an important class of anion channels that are opened by increases in cytosolic [Ca2+]. Here, we examine the mechanisms of anion permeation through ClCaCs from Xenopus oocytes in excised inside-out and outside-out patches. ClCaCs exhibited moderate selectivity for Cl over Na: PNa/PCl = 0.1. The apparent affinity of ClCaCs for Cl was low: Kd = 73 mM. The channel had an estimated pore diameter >0.6 nm. The relative permeabilities measured under bi-ionic conditions by changes in Erev were as follows: C(CN)3 > SCN > N(CN)2 > ClO4 &
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9

Franciolini, F., and W. Nonner. "A multi-ion permeation mechanism in neuronal background chloride channels." Journal of General Physiology 104, no. 4 (1994): 725–46. http://dx.doi.org/10.1085/jgp.104.4.725.

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Unitary current/voltage relationships of background Cl channels of rat hippocampal neurons were determined for varied gradients and absolute concentrations of NaCl. The channels revealed permeabilities for both Cl and Na ions. A hyperlinear increase of unitary conductance, observed for a symmetrical increase of salt concentration from 300 and 600 mM, indicated a multi-ion permeation mechanism. A variety of kinetic models of permeation were tested against the experimental current/voltage relationships. Models involving a pore occupied by mixed complexes of up to five ions were necessary to repr
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10

Stutzin, Andrés, Rubén Torres, Macarena Oporto, et al. "Separate taurine and chloride efflux pathways activated during regulatory volume decrease." American Journal of Physiology-Cell Physiology 277, no. 3 (1999): C392—C402. http://dx.doi.org/10.1152/ajpcell.1999.277.3.c392.

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Organic osmolyte and halide permeability pathways activated in epithelial HeLa cells by cell swelling were studied by radiotracer efflux techniques and single-cell volume measurements. The replacement of extracellular Cl− by anions that are more permeant through the volume-activated Cl− channel, as indicated by electrophysiological measurements, significantly decreased taurine efflux. In the presence of less-permeant anions, an increase in taurine efflux was observed. Simultaneous measurement of the125I, used as a tracer for Cl−, and [3H]taurine efflux showed that the time courses for the two
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11

Betto, Giulia, O. Lijo Cherian, Simone Pifferi, Valentina Cenedese, Anna Boccaccio, and Anna Menini. "Interactions between permeation and gating in the TMEM16B/anoctamin2 calcium-activated chloride channel." Journal of General Physiology 143, no. 6 (2014): 703–18. http://dx.doi.org/10.1085/jgp.201411182.

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At least two members of the TMEM16/anoctamin family, TMEM16A (also known as anoctamin1) and TMEM16B (also known as anoctamin2), encode Ca2+-activated Cl− channels (CaCCs), which are found in various cell types and mediate numerous physiological functions. Here, we used whole-cell and excised inside-out patch-clamp to investigate the relationship between anion permeation and gating, two processes typically viewed as independent, in TMEM16B expressed in HEK 293T cells. The permeability ratio sequence determined by substituting Cl− with other anions (PX/PCl) was SCN− > I− > NO3− &am
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12

Voets, Thomas, Guy Droogmans, and Bernd Nilius. "Modulation of Voltage-dependent Properties of a Swelling-activated Cl− Current." Journal of General Physiology 110, no. 3 (1997): 313–25. http://dx.doi.org/10.1085/jgp.110.3.313.

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We used the patch-clamp technique to study the voltage-dependent properties of the swelling-activated Cl− current (ICl,swell) in BC3H1 myoblasts. This Cl− current is outwardly rectifying and exhibits time-dependent inactivation at positive potentials (potential for half-maximal inactivation of +75 mV). Single-channel Cl− currents with similar voltage-dependent characteristics could be measured in outside-out patches pulled from swollen cells. The estimated single-channel slope conductance in the region between +60 and +140 mV was 47 pS. The time course of inactivation was well described by a d
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13

Smith, Stephen S., Erich D. Steinle, Mark E. Meyerhoff, and David C. Dawson. "Cystic Fibrosis Transmembrane Conductance Regulator." Journal of General Physiology 114, no. 6 (1999): 799–818. http://dx.doi.org/10.1085/jgp.114.6.799.

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The cystic fibrosis transmembrane conductance regulator (CFTR) Cl channel exhibits lyotropic anion selectivity. Anions that are more readily dehydrated than Cl exhibit permeability ratios (PS/PCl) greater than unity and also bind more tightly in the channel. We compared the selectivity of CFTR to that of a synthetic anion-selective membrane [poly(vinyl chloride)–tridodecylmethylammonium chloride; PVC-TDMAC] for which the nature of the physical process that governs the anion-selective response is more readily apparent. The permeability and binding selectivity patterns of CFTR differed only by a
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14

Halm, D. R., and R. A. Frizzell. "Anion permeation in an apical membrane chloride channel of a secretory epithelial cell." Journal of General Physiology 99, no. 3 (1992): 339–66. http://dx.doi.org/10.1085/jgp.99.3.339.

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Single channel currents though apical membrane Cl channels of the secretory epithelial cell line T84 were measured to determine the anionic selectivity and concentration dependence of permeation. The current-voltage relation was rectified with single channel conductance increasing at positive potentials. At 0 mV the single channel conductance was 41 +/- 2 pS. Permeability, determined from reversal potentials, was optimal for anions with diameters between 0.4 and 0.5 nm. Anions of larger diameter had low permeability, consistent with a minimum pore diameter of 0.55 nm. Permeability for anions o
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15

Steinberg, Benjamin E., Kassidy K. Huynh, Alexandre Brodovitch, et al. "A cation counterflux supports lysosomal acidification." Journal of Cell Biology 189, no. 7 (2010): 1171–86. http://dx.doi.org/10.1083/jcb.200911083.

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The profound luminal acidification essential for the degradative function of lysosomes requires a counter-ion flux to dissipate an opposing voltage that would prohibit proton accumulation. It has generally been assumed that a parallel anion influx is the main or only counter-ion transport that enables acidification. Indeed, defective anion conductance has been suggested as the mechanism underlying attenuated lysosome acidification in cells deficient in CFTR or ClC-7. To assess the individual contribution of counter-ions to acidification, we devised means of reversibly and separately permeabili
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16

Fykse, E. M., та F. Fonnum. "Transport of γ-aminobutyrate and l-glutamate into synaptic vesicles. Effect of different inhibitors on the vesicular uptake of neurotransmitters and on the Mg2+-ATPase". Biochemical Journal 276, № 2 (1991): 363–67. http://dx.doi.org/10.1042/bj2760363.

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The uptakes of gamma-aminobutyrate (GABA) and L-glutamate into synaptic vesicles isolated from rat brain were compared with respect to the effects of 4-acetamido-4′-isothiocyanostilbene-2,2′- disulphonic acid (SITS), 4,4′-di-isothiocyanostilbene-2,2′-disulphonic acid (DIDS) and 5-nitro-2-(3-phenylpropylamino)benzoic acid (N144), agents known to block anion channels. The uptake of glutamate was inhibited by low micromolar concentrations of SITS, DIDS and N144. GABA uptake was much less sensitive to these agents than was glutamate uptake. SITS and N144 inhibited the vacuolar H(+)-ATPase of synap
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17

Franciolini, F., and W. Nonner. "Anion-cation interactions in the pore of neuronal background chloride channels." Journal of General Physiology 104, no. 4 (1994): 711–23. http://dx.doi.org/10.1085/jgp.104.4.711.

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Background Cl channels in neurons and skeletal muscle are significantly permeable for alkali cations when tested with asymmetrical concentrations of the same salt. Both anion and cation permeation were proposed to require binding of an alkali cation with the pore (Franciolini, F., and W. Nonner. 1987. Journal of General Physiology. 90:453-478). We tested this hypothesis by bilaterally substituting large alkali cations for Na and found no significant changes of unitary conductance at 300 mM symmetrical concentrations. In addition, all organic cations examined were permeant in a salt gradient te
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18

Zhou, Shi-Sheng, Zhan Gao, Ling Dong, et al. "Anion channels influence ECC by modulating L-type Ca2+ channel in ventricular myocytes." Journal of Applied Physiology 93, no. 5 (2002): 1660–68. http://dx.doi.org/10.1152/japplphysiol.00220.2002.

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Anion channels are extensively expressed in the heart, but their roles in cardiac excitation-contraction coupling (ECC) are poorly understood. We, therefore, investigated the effects of anion channels on cardiac ventricular ECC. Edge detection, fura 2 fluorescence measurements, and whole cell patch-clamp techniques were used to measure cell shortening, the intracellular Ca2+ transient, and the L-type Ca2+ current ( I Ca,L) in single rat ventricular myocytes. The anion channel blockers 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and niflumic acid reversibly inhibited the Ca2+ transients
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19

Skott, O., and B. L. Jensen. "Involvement of chloride in renin secretion from isolated rat glomeruli." American Journal of Physiology-Renal Physiology 262, no. 3 (1992): F403—F410. http://dx.doi.org/10.1152/ajprenal.1992.262.3.f403.

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The sensitivity of renin release to changes in anion and calcium concentrations was assessed in superfused rat glomeruli with attached juxtaglomerular cells. Isosmotic substitution of Cl-with gluconate (1/12, 1/6, 1/3, 2/3, or total exchange), isethionate (15 or 101 mM), or sulfate (10 mM) inhibited renin release reversibly. Substitution of Cl- with nitrate (101 mM) stimulated renin secretion. Substitution with iodide (15 or 101 mM) had no consistent effect. The stimulation induced by calcium-free solutions was high in May and low in September. In the absence of chloride, the response to calci
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20

Qu, Zhiqiang, Rodolphe Fischmeister, and Criss Hartzell. "Mouse Bestrophin-2 Is a Bona fide Cl− Channel." Journal of General Physiology 123, no. 4 (2004): 327–40. http://dx.doi.org/10.1085/jgp.200409031.

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Bestrophins have recently been proposed to comprise a new family of Cl− channels. Our goal was to test whether mouse bestrophin-2 (mBest2) is a bona fide Cl− channel. We expressed mBest2 in three different mammalian cell lines. mBest2 was trafficked to the plasma membrane as shown by biotinylation and immunoprecipitation, and induced a Ca2+-activated Cl− current in all three cell lines (EC50 for Ca2+ = 230 nM). The permeability sequence was SCN−: I−: Br−: Cl−: F− (8.2: 1.9: 1.4: 1: 0.5). Although SCN− was highly permeant, its conductance was ∼10% that of Cl− and SCN− blocked Cl− conductance (I
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21

Qu, Zhiqiang, and Criss Hartzell. "Determinants of Anion Permeation in the Second Transmembrane Domain of the Mouse Bestrophin-2 Chloride Channel." Journal of General Physiology 124, no. 4 (2004): 371–82. http://dx.doi.org/10.1085/jgp.200409108.

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Bestrophins have been proposed to constitute a new family of Cl channels that are activated by cytosolic Ca. We showed previously that mutation of serine-79 to cysteine in mouse bestrophin-2 (mBest2) altered the relative permeability and conductance to SCN. In this paper, we have overexpressed various mutant constructs of mBest2 in HEK-293 cells to explore the contributions to anion selectivity of serine-79 and other amino acids (V78, F80, G83, F84, V86, and T87) located in the putative second transmembrane domain (TMD2). Residues selected for mutagenesis were distributed throughout TMD2, but
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22

Thomas, S. A., and R. I. Hume. "Permeation of both cations and anions through a single class of ATP-activated ion channels in developing chick skeletal muscle." Journal of General Physiology 95, no. 4 (1990): 569–90. http://dx.doi.org/10.1085/jgp.95.4.569.

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Micromolar concentrations of extracellular adenosine 5'-triphosphate (ATP) elicit a rapid excitatory response in developing chick skeletal muscle. Excitation is the result of a simultaneous increase in membrane permeability to sodium, potassium, and chloride ions. In the present study we quantify the selectivity of the ATP response, and provide evidence that a single class of ATP-activated ion channels conducts both cations and anions. Experiments were performed on myoballs using the whole-cell patch-clamp technique. We estimated permeability ratios by measuring the shift in reversal potential
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23

Beblo, Dolores A., and Richard D. Veenstra. "Monovalent Cation Permeation through the Connexin40 Gap Junction Channel." Journal of General Physiology 109, no. 4 (1997): 509–22. http://dx.doi.org/10.1085/jgp.109.4.509.

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The unitary conductances and permeability sequences of the rat connexin40 (rCx40) gap junction channels to seven monovalent cations and anions were studied in rCx40-transfected neuroblastoma 2A (N2A) cell pairs using the dual whole cell recording technique. Chloride salt cation substitutions (115 mM principal salt) resulted in the following junctional maximal single channel current-voltage relationship slope conductances (γj in pS): CsCl (153), RbCl (148), KCl (142), NaCl (115), LiCl (86), TMACl (71), TEACl (63). Reversible block of the rCx40 channel was observed with TBA. Potassium anion salt
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24

Pusch, Michael, Uwe Ludewig, Annett Rehfeldt, and Thomas J. Jentsch. "Gating of the voltage-dependent chloride channel CIC-0 by the permeant anion." Nature 373, no. 6514 (1995): 527–31. http://dx.doi.org/10.1038/373527a0.

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25

Kolen, Bettina, Daniel Kortzak, Arne Franzen, and Christoph Fahlke. "An amino-terminal point mutation increases EAAT2 anion currents without affecting glutamate transport rates." Journal of Biological Chemistry 295, no. 44 (2020): 14936–47. http://dx.doi.org/10.1074/jbc.ra120.013704.

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Excitatory amino acid transporters (EAATs) are prototypical dual function proteins that function as coupled glutamate/Na+/H+/K+ transporters and as anion-selective channels. Both transport functions are intimately intertwined at the structural level: Secondary active glutamate transport is based on elevator-like movements of the mobile transport domain across the membrane, and the lateral movement of this domain results in anion channel opening. This particular anion channel gating mechanism predicts the existence of mutant transporters with changed anion channel properties, but without altera
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26

Payne, J. A., C. Lytle, and T. J. McManus. "Foreign anion substitution for chloride in human red blood cells: effect on ionic and osmotic equilibria." American Journal of Physiology-Cell Physiology 259, no. 5 (1990): C819—C827. http://dx.doi.org/10.1152/ajpcell.1990.259.5.c819.

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In human red blood cells, when chloride was replaced isosmotically with a permeant chaotropic anion of the lyotropic series (NO3, I, or SCN), an immediate and significant loss of cell water was observed. In contrast, replacement of chloride by a substituted monovalent sulfonate, such as methanesulfonate or sulfamate, had no significant effect on cell water. Cell water loss in the presence of lyotropic anions was not the result of hemolysis or cation loss but was associated with a significant fall in the distribution ratios of protons (out/in) and chloride (in/out), suggesting an increase in no
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27

Donaldson, P. J., L. K. Chen, and S. A. Lewis. "Effects of serosal anion composition on the permeability properties of rabbit urinary bladder." American Journal of Physiology-Renal Physiology 256, no. 6 (1989): F1125—F1134. http://dx.doi.org/10.1152/ajprenal.1989.256.6.f1125.

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This study describes the effects of serosal Cl- and HCO3- substitution on transepithelial Na+ transport and basolateral membrane properties of the rabbit urinary bladder. Replacement of Cl- with NO3-, SCN-, and Br- had no effect on transepithelial Na+ transport or the basolateral membrane potential (Vbl). However, gluconate, isethionate, and cyclamate (anions that were shown previously to be not as permeable as Cl- through the basolateral membrane anion channel), decreased transepithelial Na+ transport and depolarized Vbl. Replacement of HCO3- also produced a decrease in transepithelial Na+ tr
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28

Steinberg, Benjamin E., Alexandre Brodovitch, Kassidy K. Huynh, and Sergio Grinstein. "ROLE OF THE CYSTIC FIBROSIS TRANSMEMBRANE REGULATOR (CFTR) CHLORIDE CHANNEL IN MACROPHAGE LYSOSOME ACIDIFICATION." Clinical & Investigative Medicine 31, no. 4 (2008): 23. http://dx.doi.org/10.25011/cim.v31i4.4828.

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Background: Lysosome acidification is the result of proton pumping by thevacuolar-type ATPase (V-ATPase). Because the V-ATPase is electrogenic, a substantial lysosomal membrane potential can develop if left uncompensated by counterions. An increasing membrane potential will oppose further proton pumping, limiting the acidification. It has generally been assumed that a parallel anion influx accompanies proton pumping to enable acidification. Indeed, defective anion channel function in cystic fibrosis (CF) has been suggested as the mechanism underlying attenuated lysosomal acidification and impa
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29

Berkowitz, L. R. "Loop diuretic and anion modification of NEM-induced K transport in human red blood cells." American Journal of Physiology-Cell Physiology 258, no. 4 (1990): C622—C629. http://dx.doi.org/10.1152/ajpcell.1990.258.4.c622.

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The thioalkylating agent N-ethylmaleimide (NEM) causes ouabain-insensitive K loss from human red blood cells. This K loss is inhibited when intracellular Cl is replaced by another permeant anion or when loop diuretics are placed in the incubation medium after NEM exposure. In this report, we have tested the possibility that Cl replacement or loop diuretics not only influence the transport of K induced by NEM but also the interaction of NEM with its target sulfhydryl group. This possibility was examined by replacing intracellular Cl or exposing the cells to loop diuretics before NEM exposure, t
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30

Wilson, Martin, and Evanna Gleason. "An unusual voltage-gated anion channel found in the cone cells of the chicken retina." Visual Neuroscience 6, no. 1 (1991): 19–23. http://dx.doi.org/10.1017/s0952523800000870.

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AbstractUsing the whole-cell patch clamp technique, we have examined the voltage-gated currents present in adult chicken cone cells. When calcium and calcium-gated currents are blocked, hyperpolarizing voltage steps elicit slowly increasing inward currents as has been shown for photoreceptors in other species. Unlike the case for other species, chicken cones appear to lack the inward-rectifying cationic current Ih that contributes to the shaping of the photovoltage. Instead of Ih, these cones possess an anionic inward-rectifying current that in kinetics, activation range and probably function
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31

Musch, M. W., T. R. Leffingwell, and L. Goldstein. "Band 3 modulation and hypotonic-stimulated taurine efflux in skate erythrocytes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 1 (1994): R65—R74. http://dx.doi.org/10.1152/ajpregu.1994.266.1.r65.

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Previous studies have shown that exposure of skate erythrocytes to hypotonic medium or isosmotic medium with permeant solutes such as ethylene glycol or ammonium chloride increases cell volume. Initial swelling is followed by a regulatory volume decrease accomplished by efflux of cell solutes, including the beta-amino acid taurine. Taurine efflux, as well as the cell volume recovery, is inhibited by stilbene disulfonates and other anion exchange inhibitors, suggesting involvement of the erythrocyte anion exchanger band 3. In the present study we show that binding of the stilbene dihydro 4,4'-d
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32

Laver, Derek R., and Katherine M. Bradley. "Disulfonic stilbene permeation and block of the anion channel from the sarcoplasmic reticulum of rabbit skeletal muscle." American Journal of Physiology-Cell Physiology 290, no. 6 (2006): C1666—C1677. http://dx.doi.org/10.1152/ajpcell.00299.2005.

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Block of a sarcoplasmic reticulum anion channel (SCl channel) by disulfonic stilbene derivatives [DIDS, dibenzamidostilbene-2,2′-disulfonic acid (DBDS), and 4,4′-dinitrostilbene-2,2′-disulfonic acid (DNDS)] was investigated in planar bilayers using SO[Formula: see text] as the conducting ion. All molecules caused reversible voltage-dependent channel block when applied to either side of the membrane. DIDS also produced nonreversible channel block from both sides within 1–3 min. Reversible inhibition was associated with a decrease in channel open probability and mean open duration but not with a
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33

Rubaiy, Hussein N., and Paul Linsdell. "Location of a permeant anion binding site in the cystic fibrosis transmembrane conductance regulator chloride channel pore." Journal of Physiological Sciences 65, no. 3 (2015): 233–41. http://dx.doi.org/10.1007/s12576-015-0359-6.

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34

Nguyen, Dung, Hwoi Kwon, and Tsung-Yu Chen. "Divalent Cation Modulation of Ion Permeation in TMEM16 Proteins." International Journal of Molecular Sciences 22, no. 4 (2021): 2209. http://dx.doi.org/10.3390/ijms22042209.

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Intracellular divalent cations control the molecular function of transmembrane protein 16 (TMEM16) family members. Both anion channels (such as TMEM16A) and phospholipid scramblases (such as TMEM16F) in this family are activated by intracellular Ca2+ in the low µM range. In addition, intracellular Ca2+ or Co2+ at mM concentrations have been shown to further potentiate the saturated Ca2+-activated current of TMEM16A. In this study, we found that all alkaline earth divalent cations in mM concentrations can generate similar potentiation effects in TMEM16A when applied intracellularly, and that ma
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35

Serrano, José R., Xuehong Liu, Erik R. Borg, Christopher S. Alexander, C. Frank Shaw, and David C. Dawson. "CFTR: Ligand Exchange between a Permeant Anion ([Au(CN)2]−) and an Engineered Cysteine (T338C) Blocks the Pore." Biophysical Journal 91, no. 5 (2006): 1737–48. http://dx.doi.org/10.1529/biophysj.105.078899.

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36

Amorim, J. B. O., M. A. Bailey, R. Musa-Aziz, G. Giebisch, and G. Malnic. "Role of luminal anion and pH in distal tubule potassium secretion." American Journal of Physiology-Renal Physiology 284, no. 2 (2003): F381—F388. http://dx.doi.org/10.1152/ajprenal.00236.2002.

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Potassium secretory flux ( J K) by the distal nephron is regulated by systemic and luminal factors. In the present investigation, J K was measured with a double-barreled K+ electrode during paired microperfusion of superficial segments of the rat distal nephron. We used control solutions (100 mM NaCl, pH 7.0) and experimental solutions in which Cl− had been replaced with a less permeant anion and/or pH had been increased to 8.0. J K increased when Cl− was replaced by either acetate (∼37%), sulfate (∼32%), or bicarbonate (∼62%), and also when the pH of the control perfusate was increased (∼26%)
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37

Stewart, A. K., M. N. Chernova, Y. Z. Kunes, and S. L. Alper. "Regulation of AE2 anion exchanger by intracellular pH: critical regions of the NH2-terminal cytoplasmic domain." American Journal of Physiology-Cell Physiology 281, no. 4 (2001): C1344—C1354. http://dx.doi.org/10.1152/ajpcell.2001.281.4.c1344.

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The role of intracellular pH (pHi) in regulation of AE2 function in Xenopus oocytes remains unclear. We therefore compared AE2-mediated 36Cl− efflux from Xenopus oocytes during imposed variation of extracellular pH (pHo) or variation of pHi at constant pHo. Wild-type AE2-mediated 36Cl−efflux displayed a steep pHo vs. activity curve, with pHo(50) = 6.91 ± 0.04. Sequential NH2-terminal deletion of amino acid residues in two regions, between amino acids 328 and 347 or between amino acids 391 and 510, shifted pHo(50) to more acidic values by nearly 0.6 units. Permeant weak acids were then used to
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38

Bekar, Lane K., and Wolfgang Walz. "Evidence for Chloride Ions as Intracellular Messenger Substances in Astrocytes." Journal of Neurophysiology 82, no. 1 (1999): 248–54. http://dx.doi.org/10.1152/jn.1999.82.1.248.

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Cultured rat hippocampal astrocytes were used to investigate the mechanism underlying the suppression of Ba2+-sensitive K+ currents by GABAAreceptor activation. Muscimol application had two effects on whole cell currents: opening of the well-known Cl− channel of the GABAA receptor and a secondary longer-lasting blockade of outward K+ currents displaying both peak and plateau phases. This blockade was independent of both Na+ (inside and outside) and ATP in the pipette. It also seemed to be independent of muscimol binding to the receptor because picrotoxin application showed no effect on the K+
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39

Yi, Sheng, Fernando Pierucci-Alves та Bruce D. Schultz. "Transforming growth factor-β1 impairs CFTR-mediated anion secretion across cultured porcine vas deferens epithelial monolayer via the p38 MAPK pathway". American Journal of Physiology-Cell Physiology 305, № 8 (2013): C867—C876. http://dx.doi.org/10.1152/ajpcell.00121.2013.

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The goal of this study was to determine whether transforming growth factor-β1 (TGF-β1) affects epithelial cells lining the vas deferens, an organ that is universally affected in cystic fibrosis male patients. In PVD9902 cells, which are derived from porcine vas deferens epithelium, TGF-β1 exposure significantly reduced short-circuit current ( Isc) stimulated by forskolin or a cell membrane-permeant cAMP analog, 8-pCPT-cAMP, suggesting that TGF-β1 affects targets of the cAMP signaling pathway. Electrophysiological results indicated that TGF-β1 reduces the magnitude of current inhibited by cysti
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40

Halperin, J. A., C. Brugnara, M. T. Tosteson, T. Van Ha, and D. C. Tosteson. "Voltage-activated cation transport in human erythrocytes." American Journal of Physiology-Cell Physiology 257, no. 5 (1989): C986—C996. http://dx.doi.org/10.1152/ajpcell.1989.257.5.c986.

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We report here the effects of membrane potential on the permeability of the human erythrocyte to Na, K, and Ca. Membrane potential was changed either by varying the K concentration gradient in the presence of valinomycin or by varying the concentration gradient of the permeant anion nitrate in the presence of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. When the membrane potential was changed from inside negative (-10 mV) to inside positive (greater than 40 mV), influx, efflux, and net flux of Na and K increased. Marked net cation loss and cell shrinkage occurred in the absence of a chemi
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41

O'Brodovich, H., X. Wang, C. Li, B. Rafii, J. Correa, and C. Bear. "Novobiocin forms cation-permeable ion channels in rat fetal distal lung epithelium." American Journal of Physiology-Cell Physiology 264, no. 6 (1993): C1532—C1537. http://dx.doi.org/10.1152/ajpcell.1993.264.6.c1532.

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The antibiotic novobiocin has been previously reported to increase Na+ transport in frog skin, presumably by attenuation of Na+ self-inhibition of Na+ channels. To determine whether novobiocin had similar effects and utilized a similar mechanism in mammalian Na(+)-transporting tissues, we studied its effect on ion transport by primary cultures of fetal distal lung epithelium (FDLE) cultured from 20-day gestationally aged rats (term = 22 days). Novobiocin (10 mM) increased short-circuit current and markedly decreased the resistance in FDLE monolayers mounted in Ussing chambers. Fura-2 single-ce
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42

Mangoo-Karim, R., M. Ye, D. P. Wallace, J. J. Grantham, and L. P. Sullivan. "Anion secretion drives fluid secretion by monolayers of cultured human polycystic cells." American Journal of Physiology-Renal Physiology 269, no. 3 (1995): F381—F388. http://dx.doi.org/10.1152/ajprenal.1995.269.3.f381.

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We have investigated the hypothesis that active anion transport drives fluid secretion by the cystic epithelium in autosomal dominant polycystic kidney disease (ADPKD). We prepared monolayers of a primary culture derived from cystic tissue removed from ADPKD patients. The monolayers were grown on permeant supports, and fluid secretion was initiated by forskolin. The results were compared with those obtained with monolayers of Madin-Darby canine kidney (MDCK) cells, known to secrete Cl-. In the absence of the agonist, ADPKD monolayers absorbed fluid (0.20 +/- 0.02 microliter.cm surface area-2.h
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43

Takuma, T., T. Ichida, K. Okumura, Y. Sasaki, and M. Kanazawa. "Effects of valinomycin on osmotic lysis of zymogen granules and amylase exocytosis from parotid acini." American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no. 5 (1993): G895—G901. http://dx.doi.org/10.1152/ajpgi.1993.264.5.g895.

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The role of osmotic swelling of the secretory granules in adenosine 3',5'-cyclic monophosphate (cAMP)-mediated amylase exocytosis was evaluated by use of isolated zymogen granules and saponin-permeabilized acini of the rat parotid gland. The osmotic lysis of the isolated granules was markedly enhanced by the addition of valinomycin (> 10(-9) M) in the presence of isosmotic KSCN or KI medium. However, valinomycin (up to 10(-5) M) did not increase the granule lysis in KCl medium, although the granules were slightly less stable in KCl medium than in K2SO4 or potassium gluconate medium. Guanosi
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44

O'Donnell, M. J., J. A. Dow, G. R. Huesmann, N. J. Tublitz, and S. H. Maddrell. "Separate control of anion and cation transport in malpighian tubules of Drosophila Melanogaster." Journal of Experimental Biology 199, no. 5 (1996): 1163–75. http://dx.doi.org/10.1242/jeb.199.5.1163.

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Microelectrode measurements of basal, apical and transepithelial potentials in the Malpighian tubules of Drosophila melanogaster were obtained under a range of conditions in order to investigate whether each of the three main second messenger systems known to act in the tubules (cyclic AMP, cyclic GMP and Ca2+) acted specifically on either cation or anion transport, or whether they activated both systems. Ion-selective microelectrode determinations of K+ concentration and pH of secreted fluid allowed the role of each signalling system to be analysed further. Stimulation with cyclic nucleotides
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45

Cymes, Gisela D., and Claudio Grosman. "Identifying the elusive link between amino acid sequence and charge selectivity in pentameric ligand-gated ion channels." Proceedings of the National Academy of Sciences 113, no. 45 (2016): E7106—E7115. http://dx.doi.org/10.1073/pnas.1608519113.

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Among neurotransmitter-gated ion channels, the superfamily of pentameric ligand-gated ion channels (pLGICs) is unique in that its members display opposite permeant-ion charge selectivities despite sharing the same structural fold. Although much effort has been devoted to the identification of the mechanism underlying the cation-versus-anion selectivity of these channels, a careful analysis of past work reveals that discrepancies exist, that different explanations for the same phenomenon have often been put forth, and that no consensus view has yet been reached. To elucidate the molecular basis
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46

Matsumoto, Takayuki, Keisuke Takayanagi, Mihoka Kojima, Kumiko Taguchi, and Tsuneo Kobayashi. "Acute Exposure to Indoxyl Sulfate Impairs Endothelium-Dependent Vasorelaxation in Rat Aorta." International Journal of Molecular Sciences 20, no. 2 (2019): 338. http://dx.doi.org/10.3390/ijms20020338.

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Gut microbiota are emerging as potential contributors to the regulation of host homeostasis. Dysbiosis of the gut microbiota associated with increased intestinal permeability facilitates the passage of endotoxins and other microbial products, including indoxyl sulfate in the circulation. Although an emerging body of evidence has suggested that indoxyl sulfate is a key substance for the development of chronic kidney disease, few studies have investigated the direct association of indoxyl sulfate with vascular function. We hypothesized that indoxyl sulfate adversely affects vascular function. Ao
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47

Reenstra, W. W., and J. G. Forte. "Characterization of K+ and Cl- conductances in apical membrane vesicles from stimulated rabbit oxyntic cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 259, no. 5 (1990): G850—G858. http://dx.doi.org/10.1152/ajpgi.1990.259.5.g850.

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K+ and Cl- conductance pathways in apical membrane vesicles (SA vesicles) of stimulated oxyntic cells have been characterized. SA vesicles were prepared from rabbit fundic mucosa after stimulation of acid secretion with histamine. Conductive K+ and Cl- fluxes were assayed by several methods: by their effects on pH gradient formation by endogenous H(+)-K(+)-ATPase, by the protonophore-induced dissipation of preformed pH gradients, and by the effects of channel blockers. pH gradient formation by H(+)-K(+)-ATPase required K+ and was greatly reduced when the permeant anion chloride was replaced by
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48

Clarke, L. L., and M. C. Harline. "CFTR is required for cAMP inhibition of intestinal Na+ absorption in a cystic fibrosis mouse model." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 2 (1996): G259—G267. http://dx.doi.org/10.1152/ajpgi.1996.270.2.g259.

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Acute adenosine 3',5'-cyclic monophosphate (cAMP) stimulation of intestinal epithelium induces net transepithelial Cl- secretion and inhibits neutral coupled NaCl absorption. To investigate the role that the cystic fibrosis transmembrane conductance regulator (CFTR) plays in these events, we measured bioelectric changes and radioisotopic NaCl flux across jejunal tissues from gene-targeted cftr "knockout" mice [cftr(-/-) homozygotes] and their normal littermates [cftr(+/+) homozygotes and cftr(+/-) heterozygotes]. Before stimulation, the short-circuit current (Isc, an index of Cl- secretion) of
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49

Lamsa, Karri, and Kai Kaila. "Ionic Mechanisms of Spontaneous GABAergic Events in Rat Hippocampal Slices Exposed to 4-Aminopyridine." Journal of Neurophysiology 78, no. 5 (1997): 2582–91. http://dx.doi.org/10.1152/jn.1997.78.5.2582.

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Lamsa, Karri and Kai Kaila. Ionic mechanisms of spontaneous GABAergic events in rat hippocampal slices exposed to 4-aminopyridine. J. Neurophysiol. 78: 2582–2591, 1997. Ion-selective (H+ and K+) microelectrode techniques as well as conventional extra- and intracellular recordings were used to study the ionic mechanisms of propagating spontaneous GABAergic events (SGEs) in rat hippocampal slices exposed to 4-aminopyridine (4-AP, 50–100 μM). All experiments were made in the presence of antagonists of ionotropic glutamate receptors [10 μM 6-nitro-7-sulphamoylbenzoquinoxaline-2,3-dione (NBQX) and
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50

Herness, M. S. "Neurophysiological and biophysical evidence on the mechanism of electric taste." Journal of General Physiology 86, no. 1 (1985): 59–87. http://dx.doi.org/10.1085/jgp.86.1.59.

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The phenomenon of electric taste was investigated by recording from the chorda tympani nerve of the rat in response to both electrical and chemical stimulations of the tongue with electrolytes in order to gain some insight into its mechanism on both a neurophysiological and biophysical basis. The maximum neural response levels were identical for an individual salt (LiCl, NaCl, KCl, or CaCl2), whether it was presented as a chemical solution or as an anodal stimulus through a subthreshold solution. These observations support the idea that stimulation occurs by iontophoresis of ions to the recept
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