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PubMed2004

Electrochemical detection of chloride by underpotentially deposited silver films on polycrystalline gold.

This paper describes an electrochemical method for measuring dilute levels of chloride using an underpotentially deposited (UPD) Ag adlayer on polycrystalline Au substrates as a sensing agent. Specifically, chloride ions adsorb onto the Ag UPD adlayer and effect changes in the electrochemical deposition and stripping characteristics of the silver film. Cyclic voltammograms (CVs) of the native Au/Ag(UPD) electrode in 0.1 M H2SO4(aq) exhibit a primary stripping peak for the Ag UPD adlayer at 550 mV vs Ag(+/0), and chloride adsorption onto the Au/Ag(UPD) surface effects a peak shift to approximately 600 mV vs Ag(+/0), depending on the amount of adsorbed Cl-, as affected by the Cl- concentrations and contact times employed in the derivatization. The chloride-treated electrodes also exhibit a stripping peak at 275 mV that is not observed on the native substrate and increases in intensity with Cl- concentration and derivatization time. The integrated charge density for this latter stripping peak relative to that for the primary stripping peak at 550-610 mV provides a useful metric for quantifying adsorbed Cl- levels, and these values allow measurement of Cl- concentrations in dilute aqueous solutions. For Cl- concentrations between 0.5 and 100 microM, the kinetics of Cl- adsorption followed a transient Langmuir adsorption model and allowed measured surface coverages to be used for determining Cl- solution concentrations. Using contact times of 1 min for Cl- adsorption, the electrodes showed a linear response across Cl- concentrations of 0.5-20 microM.

Adsorption↗
PubMed1971

The role of sodium and calcium ions in the hypothalamus in the control of body temperature of the unanaesthetized cat.

1. Isolated regions of the anterior, posterior and other areas of the hypothalamus of the unanaesthetized cat were perfused by means of push-pull cannulae lowered through permanently implanted guide tubes. Each site was perfused for a 30 min interval at a rate of 50 mul./min. Concentrations of sodium, calcium, potassium and magnesium ions in the perfusate were altered selectively.2. Sodium ions in a concentration which varied from 13.6 to 68.0 mM in excess of the level in extracellular fluid caused a steep rise in the temperature of the cat when the solution was perfused at sites located within the posterior hypothalamic area. Shivering, vasoconstriction, and piloerection accompanied the increase in temperature. When the chloride was replaced in the perfusate by the toluene-p-sulphonate salt of sodium, the hyperthermia was equally intense. Solutions containing excess sodium ions perfused within the anterior and other hypothalamic areas produced either a slight fall or rise in temperature as well as other physiological changes.3. Calcium ions in a concentration which varied from 2.6 to 10.4 mM in excess of the physiological level perfused at the same sites within the posterior region of the hypothalamus produced a sharp fall in body temperature, which was accompanied by vasodilatation and a decrease in the activity of the cat. When solutions containing excess calcium were perfused in the anterior and other hypothalamic areas, no consistent change in temperature occurred.4. Potassium or magnesium ions in concentrations which varied from two to ten times the level in extracellular fluid had virtually no effect on the temperature of the cat when they were perfused in the anterior, posterior or other areas of the hypothalamus.5. We conclude that the constancy in the ratio between sodium and calcium ions in the posterior hypothalamus may be the inherent mechanism by which the set-point for body temperature is determined.

Animals↗
PubMed2006

Determination of perchlorate in drinking water by ion chromatography using macrocycle-based concentration and separation methods.

Macrocycle-based ion chromatography provides a convenient, reliable method for the determination of perchlorate ion, which is currently of great interest to the environmental community. This study shows that effective perchlorate determinations can be made using standard conductimetric detection by combining an 18-crown-6-based mobile phase with an underivatized reversed-phase mobile phase ion chromatography (MPIC) column. One unique feature of this method is the flexibility in column capacity that is achieved through simple variations in eluent concentrations of 18-crown-6 and KOH, facilitating the separation of target analyte anions such as perchlorate. Using a standard anion exchange column as concentrator makes possible the determination of perchlorate as low as 0.2 ug/L in low ionic strength matrices. Determination of perchlorate at the sub-ug/L level in pure water and in spiked local city hard water samples with high background ion concentrations can be achieved this way. However, like other IC techniques, this method is challenged to achieve analyses at the ug/L level in the demanding high ionic strength matrix described by the United States Environmental Protection Agency (EPA) (1,000 mg/L chloride, sulfate and carbonate). We approached this challenge by use of the Cryptand C1 concentrator column, provided by Dionex Corporation, to effectively preconcentrate perchlorate while reducing background ion concentrations in the high ionic strength matrix. The retention characteristics of the concentrator column were studied in order to maximize its effectiveness for perchlorate determinations. The method makes possible the determination of perchlorate at the 5 ug/L level in the highest ionic strength matrix described by the EPA.

Chromatography, Ion Exchange↗
PubMed1977

Pancreatic acinar cells: the acetylcholine equilibrium potential and its ionic dependency.

1. Two glass micro-electrodes were inserted into neighbouring cells from rat or mouse pancreatic segments, superfused in vitro. The tip of a third glass micro-electrode, filled with 2 M-AChCl, was placed just outside the acinus under investigation. Membrane potential and resistance, and changes in these parameters in response to short pulses of ACh stimulation, were recorded.2. The resting current-voltage relationship, obtained by injecting 100 msec depolarizing or hyperpolarizing current pulses through one of the intracellular micro-electrodes and recording the membrane potential with the other intracellular electrode, was linear within the range -5 to -60 mV.3. Injecting depolarizing or hyperpolarizing current (d.c.) through one of the intracellular micro-electrodes, the membrane potential (as measured with the other intracellular micro-electrode) could be set at various levels. The effect of ACh at different membrane potentials was investigated. When the acinar cell membrane was hyperpolarized, the amplitude of ACh-evoked depolarization was increased, while ACh-evoked depolarization was reduced when the membrane potential was reduced by depolarizing current, and finally changed into a hyperpolarization at very low membrane potentials. In each acinus investigated (rat and mouse), there was a linear relationship between amplitude of ACh-evoked potential change (DeltaV) (+ value or - value according to polarity) and resting membrane potential. During superfusion with control solution, the value of the membrane potential at which ACh did not evoke a potential change (E(ACh)) was about -15 mV in the mouse and about -20 mV in the rat. During superfusion with a chloride-free sulphate-containing solution (steady state), a linear relationship between DeltaV and resting membrane potential was again found but E(ACh) (mouse) was about +10 mV.4. A continuous rough estimate of E(ACh) was obtained by injecting repetitively depolarizing current pulses (100 msec) through one intracellular micro-electrode; in this way, the effect of ACh measured by the other intracellular electrode could be assessed simultaneously at the spontaneous resting level, and at a depolarized level. The direction of change in E(ACh) following acute changes in the superfusion fluid ion composition was assessed. Replacing extracellular chloride by sulphate caused an immediate change in E(ACh) in the positive direction. Re-admission of chloride, after a long period of chloride ion deprivation, caused an immediate sharp change in E(ACh) in the negative direction. Replacing extracellular sodium by Tris caused an immediate transient negative change in E(ACh). In contrast, taking away extracellular calcium changed E(ACh) in a positive direction. Augmenting extracellular potassium concentration to 40 mM caused a change in E(ACh) in the positive direction.5. At a membrane potential (V) equal to E(ACh) the sum of ionic currents evoked by the action of ACh is zero. Using the Goldman treatment, it appears that ACh increases membrane Na, K and Cl permeability. The approximate relative ion permeabilities of the pathways opened up by ACh are: P(Na)/P(K) = 2.5 and P(Cl)/P(K) = 5. At V = E(ACh), the approximate relative sizes of the ACh-evoked currents are: I(Na)/I(K) = 2.6 and I(Cl)/I(K) = 1.6 ACh, therefore, causes influx of Na and Cl and a small efflux of K.

Acetylcholine↗
PubMed1995

Octreotide inhibition of serotonin-induced ileal chloride secretion.

Octreotide (SMS, synthetic miniature somatostatin) effectively alleviates the secretory diarrhea of the malignant carcinoid syndrome. Although SMS inhibits tumor release of serotonin (5HT) and other bioactive agents, it also inhibits the diarrhea in patients who continue to exhibit elevated serum levels of 5HT. This observation suggest that SMS may directly inhibit mediator-stimulated intestinal ion secretion at the mucosal level. To test this hypothesis, intestinal ion secretion was studied in rabbit ileal mucosa mounted in Ussing chambers. Maximal changes in short circuit current (delta Isc) were observed as an indicator of mucosal ion secretion. The application of pathophysiologic concentrations of 5HT (10(-5) M) to the mucosal preps resulted in a delta Isc of 52 +/- 6 microA/cm2. This 5HT-stimulated delta Isc was significantly inhibited by serosal furosemide (10(-3) M) or use of a chloride-depleted medium, indicating that 5HT stimulates electrogenic chloride secretion in the rabbit ileum. Pretreatment with a therapeutic concentration of SMS (10(-8) M) resulted in a significant inhibition of 5HT-stimulated electrogenic Cl- secretion (9 +/- 1 microA/cm2) (P < 0.005). This inhibitory effect of SMS was not seen in tissue pretreated with pertussis toxin. The results of these experiments demonstrate that octreotide inhibits 5HT-stimulated electrogenic chloride secretion at the mucosal level. Additionally this inhibitory effect of octreotide is likely mediated by activation of the inhibitory subunit of membrane-bound GTP-binding regulatory proteins. These results thus provide experimental evidence in support of the ability of SMS to ameliorate the carcinoid diarrhea by a direct effect on stimulated mucosal ion secretion.

Animals↗
PubMed2005

Chronic cholinergic imbalances promote brain diffusion and transport abnormalities.

Cholinergic imbalances occur after traumatic effects and in the initial stages of neurodegenerative diseases, but their long-lasting effects remained largely unexplained. To address this, we used TgS transgenic mice constitutively overexpressing synaptic acetylcholinesterase (AChE-S) and presenting a complex phenotype of progressive neurodeterioration. T1- and T2-weighted magnetic resonance (MR) brain images appeared similar. However, diffusion-weighted MRI showed decreased baseline water apparent diffusion coefficient in the brains of TgS animals. Furthermore, contrast-enhanced MRI after gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA) injection demonstrated slower recovery of normal signals in the TgS brains than with controls. Perfusion MR imaging and difference T1 maps calculated from pre- postcontrast T1-weighted MR images indicated accumulation of more Gd-DTPA molecules in the TgS brains than in the parent strain, reflecting impaired blood-brain barrier (BBB) functioning in these transgenic mice. To explore the molecular mechanism(s) underlying these global phenotypes, we performed microarray analysis in the stress-controlling prefrontal cortex of TgS vs. strain-matched wild-type animals. Profound overexpression of numerous ion channels, transporters, and adhesion genes was confirmed by real time RT-PCR tests. Immunohistochemical and immunoblot analyses revealed corresponding increases in the level and cellular distributions of the chloride channel CLCN3 and the water channel AQP4, both of which contribute to BBB maintenance. Our study attributes to balanced cholinergic neurotransmission, a central role in the brain's maintenance of water diffusion and ion transport, and indicates that chronic impairments in this maintenance facilitate neurodeterioration through interference with BBB function.

Acetylcholine↗
PubMed1998

Anionic binding site and 2,3-DPG effect in bovine hemoglobin.

It is generally believed that bovine hemoglobin (BvHb) interacts weakly with 2,3-diphosphoglycerate (2,3-DPG) in a chloride-free media and not at all in the presence of physiological concentrations of chloride (100 mM). This lack of interaction has raised several questions at both structural and evolutionary levels. Results obtained in this study via 31P nuclear magnetic resonance (NMR) show that, even in the presence of 100 mM chloride ions, 2,3-DPG does, in fact, interact with bovine deoxy-Hb. This spectroscopic observation has been confirmed by oxygen binding experiments, which have also shown that, under certain conditions, chloride and 2,3-DPG may display a synergistic effect in modifying the oxygen affinity of bovine hemoglobin. It could be that this synergistic effect has its structural basis in a conformational modification induced by 2,3-DPG, possibly causing extra chloride anions to approach the positive charges which constitute the anion binding site. Another possibility, not necessarily an alternative, is the additional chloride binding site recently identified [Fronticelli, C., Sanna, M. T., Perez-Alvarado, G. C., Karavitis, M., Lu, A.-L., and Brinnigar, W. S. (1995) J. Biol. Chem 270, 30588-30592] involving lysine beta76 that in bovine Hb substitutes for the alanine residue present in human hemoglobin. All of these findings are in agreement with the very low enthalpy of oxygenation that characterizes bovine Hb when both chloride and 2,3-DPG are present in concomitance. The results reported here clearly show that bovine hemoglobin does react with 2, 3-DPG and is functionally affected by this organic phosphate. Hence, the very low intraerythrocytic concentration of 2,3-DPG (0.5 mM) in adult bovine red blood cells is the result of metabolic adaptation which cannot be explained solely by the different amino acid sequence at the level of the 2,3-DPG binding site.

2,3-Diphosphoglycerate↗
PubMed1975

A preliminary investigation into the roles played by the rectal gland and kidneys in the osmoregulation of the striped dogfish Poroderma africanum.

Presented here are the results of a preliminary investigation into ionic and osmotic regulation by the kidneys and rectal gland of the striped dogfish, Poroderma africanum. Fish with ligated rectal glands showed an increase in blood concentration of sodium and chloride within a short time period, reaching a maximum after four days. The blood concentration of the two ions then decreased over the following ten days. Control animals showed relatively unchanged blood-sodium and chloride levels, over the entire 14-day period. After salt loading, both control animals and those with ligated rectal glands showed initial rise in blood sodium and chloride levels, but these returned towards initial values within seven hours of injection. Comparison of the two groups indicates that the rectal gland may control blood-chloride levels more so than -sodium, although its action as a salt regulator does not seem very pronounced in either case. Urine and rectal gland fluid, were collected as a compound fluid, from normal fish, and the estimated cloacal salt loss is discussed. Urine from normal fish was also collected separately and was analysed for its contribution to salt loss. Results are discussed and compared with previous relevant findings.

Animals↗
PubMed1990

Characterization of an early afterhyperpolarization after a brief train of action potentials in rat hippocampal neurons in vitro.

1. In rat hippocampal pyramidal cells in vitro, a brief train of action potentials elicited by direct depolarizing current pulses injected through an intracellular recording electrode is followed by a medium-duration afterhyperpolarization (mAHP) and a longer, slow AHP. We studied the mAHP with the use of current-clamp techniques in the presence of dibutyryl cyclic adenosine 3',5'-monophosphate (cAMP) to block the slow AHP and isolate the mAHP. 2. The mAHP evoked at hyperpolarized membrane potentials was complicated by a potential generated by the anomalous rectifier current, IQ. The mAHP is insensitive to chloride ions (Cl-), whereas it is sensitive to the extracellular potassium concentration ([K+]o). 3. At slightly depolarized levels, the mAHP is partially Ca2+ dependent, being enhanced by increased [Ca2+]o and BAY K 8644 and depressed by decreased [Ca2+]o, nifedipine, and Cd2+. The Ca2(+)-dependent component of the mAHP was also reduced by 100 microM tetraethylammonium (TEA) and charybdotoxin (CTX), suggesting it is mediated by the voltage- and Ca2(+)-dependent K+ current, IC. 4. Most of the Ca2(+)-independent mAHP was blocked by carbachol, implying that IM plays a major role. In a few cells, a small Ca2(+)- and carbachol-insensitive mAHP component was detectable, and this component was blocked by 10 mM TEA, suggesting it was mediated by the delayed rectifier current, IK. The K+ channel antagonist 4-aminopyridine (4-AP, 500 microM) did not reduce the mAHP. 5. We infer that the mAHP is a complex potential due either to IQ or to the combined effects of IM and IC. The contributions of each current depend on the recording conditions, with IC playing a role when the cells are activated from depolarized potentials and IM dominating at the usual resting potential. IQ is principally responsible for the mAHP recorded at hyperpolarized membrane potentials.

Action Potentials↗
PubMed2005

Dysfunctional cilia lead to altered ependyma and choroid plexus function, and result in the formation of hydrocephalus.

Cilia are complex organelles involved in sensory perception and fluid or cell movement. They are constructed through a highly conserved process called intraflagellar transport (IFT). Mutations in IFT genes, such as Tg737, result in severe developmental defects and disease. In the case of the Tg737orpk mutants, these pathological alterations include cystic kidney disease, biliary and pancreatic duct abnormalities, skeletal patterning defects, and hydrocephalus. Here, we explore the connection between cilia dysfunction and the development of hydrocephalus by using the Tg737orpk mutants. Our analysis indicates that cilia on cells of the brain ventricles of Tg737orpk mutant mice are severely malformed. On the ependymal cells, these defects lead to disorganized beating and impaired cerebrospinal fluid (CSF) movement. However, the loss of the cilia beat and CSF flow is not the initiating factor, as the pathology is present prior to the development of motile cilia on these cells and CSF flow is not impaired at early stages of the disease. Rather, our results suggest that loss of cilia leads to altered function of the choroid plexus epithelium, as evidenced by elevated intracellular cAMP levels and increased chloride concentration in the CSF. These data suggest that cilia function is necessary for regulating ion transport and CSF production, as well as for CSF flow through the ventricles.

Animals↗
PubMed2004

Effects of angiotensin II on the pericyte-containing microvasculature of the rat retina.

The aim of this study was to identify the mechanisms by which angiotensin II alters the physiology of the pericyte-containing microvasculature of the retina. Despite evidence that this vasoactive signal regulates capillary perfusion by inducing abluminal pericytes to contract and thereby microvascular lumens to constrict, little is known about the events linking angiotensin exposure with pericyte contraction. Here, using microvessels freshly isolated from the adult rat retina, we monitored pericyte currents via perforated-patch pipettes, measured pericyte calcium levels with fura-2 and visualized pericyte contractions and lumen constrictions by time-lapse photography. We found that angiotensin activates nonspecific cation (NSC) and calcium-activated chloride channels; the opening of these channels induces a depolarization that is sufficient to activate the voltage-dependent calcium channels (VDCCs) expressed in the retinal microvasculature. Associated with these changes in ion channel activity, intracellular calcium levels rise, pericytes contract and microvascular lumens narrow. Our experiments revealed that an influx of calcium through the NSC channels is an essential step linking the activation of AT(1) angiotensin receptors with pericyte contraction. Although not required in order for angiotensin to induce pericytes to contract, calcium entry via VDCCs serves to enhance the contractile response of these cells. In addition to activating nonspecific cation, calcium-activated chloride and voltage-dependent calcium channels, angiotensin II also causes the functional uncoupling of pericytes from their microvascular neighbours. This inhibition of gap junction-mediated intercellular communication suggests a previously unappreciated complexity in the spatiotemporal dynamics of the microvascular response to angiotensin II.

Alkaloids↗
PubMed1992

Control of CFTR chloride conductance by ATP levels through non-hydrolytic binding.

Site-specific mutation and membrane reconstitution experiments provide compelling evidence that the product of the gene which is at fault in the disease cystic fibrosis, termed the cystic fibrosis transmembrane conductance regulator (CFTR), is a small-conductance chloride channel activated by phosphorylation. As transport of chloride ions is passive, the predicted presence of two nucleotide-binding domains in CFTR seems as puzzling as a report that ATP hydrolysis is essential to activate the channel. We now find that in the sweat duct, which expresses high levels of CFTR and has a very high Cl- conductance, intracellular concentrations of ATP must be about normal (5 mM) for activation of this conductance, apparently by a non-hydrolytic, perhaps allosteric, mechanism. This passive dependence on ATP should mean that even a modest depletion of cell energy levels will significantly lower the energy demands of electrolyte transport by decreasing chloride conductance. We believe this direct coupling between cellular ATP levels and chloride channel activity is an adaptive mechanism to protect the tissue from damage resulting from excessive energy depletion.

Adenosine Triphosphate↗
PubMed1993

Chloride channels with reduced single-channel conductance in recessive myotonia congenita.

Myoballs were cultured from muscle biopsies of patients having Becker-type recessive generalized myotonia (RGM). Single-channel recordings showed that the conductance of the "intermediate" Cl- channel, the Cl- channel having the highest membrane density and accounting for most of the Cl- conductance in myoballs, was reduced to about 50%. All other channel parameters tested, such as gating properties, ion selectivity, and regulatory pathways, were not different from controls. Two other Cl- channel types were only rarely observed and did not seem different from controls. Also, the macroscopic Cl- conductance measured with tight-seal whole-cell recording was smaller than controls, particularly in the positive membrane potential domain. These results might explain myotonia in RGM on the single-channel level.

Cell Membrane↗
PubMed1993

Ionic mechanism of action of adenosine on the rat superior cervical ganglion.

1. The ionic mechanism responsible for hyperpolarization of the rat superior cervical ganglion (SCG) and depression of the depolarizing response to muscarine by adenosine was studied using an extracellular grease-gap recording technique. 2. Both the hyperpolarizations to adenosine and 2-chloroadenosine and the depression of the response to muscarine by adenosine were potentiated in reduced external calcium (Ca2+). Hyperpolarizations to adenosine were either unaltered or potentiated in the presence of the dihydropyridine Ca2+ channel antagonists, nitrendipine or (+)PN200 110 respectively. Hyperpolarizations to adenosine were unaltered by inorganic Ca2+ channel antagonists except for cobalt, which also antagonized hyperpolarizations to carbachol and depolarizations to muscarine. 3. Hyperpolarizations to adenosine were unaltered in nominally magnesium (Mg2+)-free or in reduced external chloride (Cl-) media. When sodium ions (Na+) were replaced by lithium ions (Li+) maximal responses to adenosine were initially enhanced, returning to pretreatment levels and subsequently reduced in their duration. In contrast, responses to adenosine were significantly enhanced in nominally potassium (K+)-free medium and reduced upon doubling the extracellular K+. 4. Hyperpolarizations were enhanced in the presence of the K+ channel antagonists, 4-aminopyridine and 3,4-diaminopyridine, and reduced by a low concentration (2 mM) of tetraethylammonium (TEA), but not in 10 mM TEA. 5. The results support the hypothesis that adenosine-mediated hyperpolarization of postganglionic neurones of the rat SCG is by a Ca(2+)-independent mechanism and is probably mediated via an increase of a K+ current. The results also indicate that adenosine-induced hyperpolarizations of the rat SCG are independent of the presence of extracellular magnesium.

Adenosine↗
PubMed2001

[Effect of calcium ion level in blood on physiological functions in rat subjected to immersion hypothermia].

I.v. administration of disodium salt of the ethylenediamine tetra-acetic acid to continuously immersed white rats intensified the rats' amplitude and rate of the respiration movement. I.v. administration of calcium chloride to the cooled rats diminished by 11.3% the respiration movement amplitude and by 20.7%--the muscles electrical activity. The findings confirm important role of the calcium ions in infringement of physiological functions under conditions of hypothermia.

Animals↗
PubMed1993

A point mutation in a Drosophila GABA receptor confers insecticide resistance.

Vertebrates and invertebrates both have GABA (gamma-aminobutyric acid) as a major inhibitory neurotransmitter. GABAA receptors in vertebrates assemble as heteromultimers to form an integral chloride ion channel. These receptors are targets for drugs and pesticides and are also implicated in seizure-related diseases. Picrotoxinin (PTX) and cyclodiene insecticides are GABAA receptor antagonists which competitively displace each other from the same binding site. Insects and vertebrates showing resistance to cyclodienes also show cross-resistance to PTX. Previously, we used a field-isolated Drosophila mutant Rdl (Resistant to dieldrin) insensitive to PTX and cyclodienes to clone a putative GABA receptor. Here we report the functional expression and novel pharmacology of this GABA receptor and examine the functionality of a resistance-associated point mutation (alanine to serine) within the second membrane-spanning domain, the region thought to line the chloride ion channel pore. This substitution is found globally in Drosophila populations. This mutation not only identifies a single amino acid conferring high levels of resistance to the important GABA receptor antagonist PTX but also, by conferring resistance to cyclodienes, may account for over 60% of reported cases of insecticide resistance.

Alanine↗