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PubMed1997

Taurine reduction in anaerobic respiration of Bilophila wadsworthia RZATAU.

Organosulfonates are important natural and man-made compounds, but until recently (T. J. Lie, T. Pitta, E. R. Leadbetter, W. Godchaux III, and J. R. Leadbetter. Arch. Microbiol. 166:204-210, 1996), they were not believed to be dissimilated under anoxic conditions. We also chose to test whether alkane- and arenesulfonates could serve as electron sinks in respiratory metabolism. We generated 60 anoxic enrichment cultures in mineral salts medium which included several potential electron donors and a single organic sulfonate as an electron sink, and we used material from anaerobic digestors in communal sewage works as inocula. None of the four aromatic sulfonates, the three unsubstituted alkanesulfonates, or the N-sulfonate tested gave positive enrichment cultures requiring both the electron donor and electron sink for growth. Nine cultures utilizing the natural products taurine, cysteate, or isethionate were considered positive for growth, and all formed sulfide. Two clearly different pure cultures were examined. Putative Desulfovibrio sp. strain RZACYSA, with lactate as the electron donor, utilized sulfate, aminomethanesulfonate, taurine, isethionate, and cysteate, converting the latter to ammonia, acetate, and sulfide. Strain RZATAU was identified by 16S rDNA analysis as Bilophila wadsworthia. In the presence of, e.g., formate as the electron donor, it utilized, e.g., cysteate and isethionate and converted taurine quantitatively to cell material and products identified as ammonia, acetate, and sulfide. Sulfite and thiosulfate, but not sulfate, were utilized as electron sinks, as was nitrate, when lactate was provided as the electron donor and carbon source. A growth requirement for 1,4-naphthoquinone indicates a menaquinone electron carrier, and the presence of cytochrome c supports the presence of an electron transport chain. Pyruvate-dependent disappearance of taurine from cell extracts, as well as formation of alanine and release of ammonia and acetate, was detected. We suspected that sulfite is an intermediate, and we detected desulfoviridin (sulfite reductase). We thus believe that sulfonate reduction is one aspect of a respiratory system transferring electrons from, e.g., formate to sulfite reductase via an electron transport system which presumably generates a proton gradient across the cell membrane.

Acetates↗

PubMed1995

Role of membrane-permeable ions in renin secretion by renal juxtaglomerular cells.

In this study we examine the role of membrane-permeable ions in renin secretion from renal juxtaglomerular (JG) cells. To this end, extracellular Cl- (100 mmol/l) in the culture medium of isolated mouse renal JG cells was replaced by the permeable anion NO3- or by the membrane-impermeable anion isethionate. Alternatively, extracellular Na+ (100 mmol/l) was substituted by the membrane-impermeable cation choline. The effects of these ion substitutions on basal and stimulated renin secretion were then examined. Renin secretion was stimulated by the adenylate cyclase activator forskolin (10 microM), the NO donor sodium nitroprusside (SNP, 100 microM), the calmodulin antagonist calmidazolium (10 microM), by lowering extracellular Ca2+ concentration ([Ca2+]e) with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) (2 mM), and by increasing [Ca2+]e from the normal value of 0.5 to 3 mM. Substitution of extracellular Cl- by isethionate, but not by NO3-, inhibited basal renin release over 20 h of incubation. NO3- also did not change renin secretion stimulated by forskolin, SNP, calmidazolium, EGTA, or by increased [Ca2+]e. Isethionate, on the other hand, markedly attenuated the effects of EGTA and of increased [Ca2+]e, but not the stimulatory effect of forskolin, calmidazolium, or SNP. Substitution of Na+ by choline also attenuated basal renin secretion and renin secretion stimulated by lowering or raising [Ca2+]e. These findings suggest that, with respect to the dependency on permeable ions, at least two different pathways of regulated renin secretion from JG cells exist: a cation- and anion-dependent Ca(2+)-related pathway and a less ion-sensitive pathway for renin secretion activated by adenosine 3',5'-cyclic monophosphate and NO.

Animals↗

PubMed1980

Osmotic lysis of bovine chromaffin granules in isotonic solutions of salts of weak organic acids. Release of catecholamines, ATP, dopamine beta-hydroxylase, and enkephalin-like material.

Chromaffin granules in isotonic solutions of K+ CH3COO- (acetate), K+ CH3CHOHCOO- (lactate), and K+2-OOCCH2CH2COO- (succinate) are stable at pH 7 but release 40 to 80% of their soluble contents of catecholamines, ATP, and dopamine beta-hydroxylase when the medium pH is less than 6. Enkephalin-like material which has recently been shown to co-sediment with chromaffin granules in sucrose density gradients is also released at low pH. The release of ATP and enkephalin-like material is proportional to the release of catecholamine. The release of soluble constituents of chromaffin granules is inhibited by increasing the osmolality of the solution with sucrose. Granules in isotonic solutions of salts of strong acids such as K+CH3SO4- (methylsulfate), K+ CH2OHCH2SO3- (isethionate), and K2SO4 are stable between pH7.0 and 5.4. The granules behave as predicted for organelles with an acid interior and the data provide further evidence that the intragranular pH is acidic. In addition, the results strongly suggest that enkephalin-like material is stored together with catecholamine and ATP in an acid compartment.

Acetates↗

PubMed1988

Prolactin synthesis in cultured pituitary cells is chloride-dependent.

Release of prolactin from both normal pituitary cells and rat pituitary tumor (GH) cells is an osmotic process that is dependent upon chloride. The long term growth rate of GH-cells in medium in which chloride was exchanged with isethionate was completely normal, but, by 48 h, isethionate substitution resulted in a 70% decrease in the concentration of internal and secreted prolactin. Isethionate caused a much smaller reduction in growth hormone production (less than 20%). These results suggest that exchange of chloride with isethionate is inhibiting the synthesis of prolactin. Reduction of intracellular levels of prolactin in cells grown in isethionate-containing medium was evident by 30 h, and the level of prolactin was reduced 92% at 96 h. This reduction in the internal concentrations of prolactin was reversed when the cells were returned to normal medium containing chloride with a t1/2 of 48 h. Addition of epidermal growth factor and the calcium channel agonist BAY K 8644 to cells in medium containing chloride increased internal prolactin by 400%, and isethionate exchange reduced the response by 85%. To confirm that isethionate exchange was inhibiting the synthesis of prolactin, mRNA concentrations for prolactin and actin were determined. Both basal and hormone-stimulated levels of prolactin mRNA were reduced 70 to 90% by isethionate exchange, while actin mRNA levels did not change. To determine whether the effect of isethionate was at the level of gene transcription, GH-cells were transfected with a prolactin-chloramphenicol acetyltransferase fusion gene and chloramphenicol acetyltransferase expression was assessed using cells in chloride and isethionate-containing media. Both basal and hormone-stimulated synthesis of chloramphenicol acetyltransferase driven by the prolactin promoter was inhibited by isethionate exchange. These studies demonstrate that exchange of medium chloride with isethionate inhibits the synthesis of prolactin at the level of transcription.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1985

Modulation of a GABA-ergic inhibitory circuit in the in vitro hippocampus by etomidate isomers.

A pulse-paired stimulation technique was used to examine the in vitro effects of the isomers of etomidate on synaptic transmission between Schaffer collaterals and CA1 pyramidal cells in the guinea pig hippocampus. Etomidate produced a dose-related, stereospecific, reversible increase in paired-pulse inhibition. Replacement of Cl- by isethionate reversed the inhibition induced by (+)-etomidate. Together with earlier biochemical evidence, these results show that in the mammalian CNS (+)-etomidate enhances central inhibition by increasing the effectiveness of gamma-aminobutyric acid (GABA) in a chloride-dependent fashion.

Animals↗

PubMed1990

Chloride conductance contributes to period determination of a neuronal circadian pacemaker.

The isolated eye of Bulla gouldiana, a marine mollusc, is a circadian pacemaker. Previous studies have shown that membrane potential changes of neurons at the base of the Bulla retina play a critical role in the expression of the circadian rhythm and that the free-running period can be modified by chronic alteration of the resting membrane potential. We now report that treatments which inhibit CI- conductance shorten the free-running period. Substitution of CI- with the anions SO4(2-), isethionate and glutamate significantly shorten the period of the ocular rhythm in vitro. Furthermore, addition of the CI- channel blocker 9-anthracene-carboxylic acid (9-AC) is also effective at shortening the period of the circadian rhythm. These data suggest that a CI- conductance participates in determining the free-running period of the circadian pacemaker cells. This is the first report of CI- conductance involvement in a circadian system and the effect is remarkable in that few treatments are known which reliably shorten the period of circadian clocks.

Animals↗

PubMed1983

The composition of animal cells: solutes contributing to osmotic pressure and charge balance.

The cytoplasmic solutes of vertebrates and invertebrates, other than Na, K and Cl, are surveyed in relation to their influence on ionic regulation through osmolality and charge balance. The most abundant include MgATP, phosphagens, amino acids, various other nitrogen and phosphorus compounds and sometimes anaerobic end products and antifreeze agents. Differences in muscle osmolality, e.g. between marine and non-marine animals, affect mainly nitrogenous solutes of no net charge, such as certain amino acids, taurine, betaine, trimethylamine oxide and urea. The high osmolality of axoplasm in marine invertebrates is due more to anions such as aspartate, glutamate and isethionate.

Amino Acids↗

PubMed1998

Regulation of acetylcholine release by intracellular acidification of developing motoneurons in Xenopus cell cultures.

1. The effects of intracellular pH changes on the acetylcholine (ACh) release and cytoplasmic Ca2+ concentration at developing neuromuscular synapses were studied in Xenopus nerve-muscle co-cultures. 2. Spontaneous and evoked ACh release of motoneurons was monitored by using whole-cell voltage-clamped myocytes. Intracellular alkalinization with 15 mM NH4Cl slightly reduced the frequency of spontaneous synaptic currents (SSCs). However, cytosolic acidification following withdrawal of extracellular NH4Cl caused a marked and transient increase in spontaneous ACh release. 3. Another method of cytosolic acidification was used in which NaCl in Ringer solution was replaced with weak organic acids. The increase in spontaneous ACh release paralleled the level of intracellular acidification resulting from addition of these organic acids. Acetate and propionate but not isethionate, methylsulphate and glucuronate, caused an increase in intracellular pH and a marked increase in spontaneous ACh release. 4. Impulse-evoked ACh release was slightly augmented by intracellular alkalinization and inhibited by cytosolic acidification. 5. Cytosolic acidification was accompanied by an elevation in the cytoplasmic Ca2+ concentration ([Ca2+]i), resulting from both external Ca2+ influx and intracellular Ca2+ mobilization. In contrast, the increase in [Ca2+]i induced by high K+ was inhibited by cytosolic acidification. 6. We conclude that cytosolic acidification regulates spontaneous and evoked ACh release differentially in Xenopus motoneurons, increasing spontaneous ACh release but inhibiting evoked ACh release.

Acetylcholine↗

PubMed1986

Anionic basis of fluid secretion by rat pancreatic acini in vitro.

Acinar secretion was studied in the caerulein-stimulated perfused rat pancreas. Unstimulated glands secreted at a mean basal rate of 1.1 microliters X g-1 X min-1 (SD = 0.74), which was not altered by perfusate anion substitution or by transport-blocking drugs. Caerulein evoked a maximum response (6.8 microliter X g-1 X min-1, SE = 0.36, n = 8) at a concentration of 18 pmol/l. Replacement of perfusate bicarbonate with either chloride or acetate did not significantly alter the stimulated secretory rate. In contrast, replacement with acetate of either chloride alone or chloride and bicarbonate reduced the rate of stimulated secretion by 75-80%, and replacement with isethionate abolished the response altogether. In glands perfused with solutions containing chloride but not bicarbonate, furosemide (10(-5) M), 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS, 10(-4) M), amiloride (10(-4) M), and methazolamide (10(-4) M) all reduced the secretory response by more than 70%. When bicarbonate was included in the perfusate, the inhibitory effects for the same doses of blockers were much less, and except for methazolamide the same level of maximum inhibition was obtained when the blocker doses were increased 10-fold. The results suggest that rat pancreatic acini utilize a different secretory mechanism from the sodium chloride-carrying symport postulated to be most important in rat mandibular glands. The simplest model to explain our results would involve paired, basolateral antiports for Na-H and Cl-HCO3 exchange. We cannot exclude the presence of a Na-Cl symport, but if present, its role appears to be minor.

Acetates↗

PubMed1993

Cl- channels in basolateral renal medullary membranes: VII. Characterization of the intracellular anion binding sites.

A unique property of basolateral membrane Cl- channels from the mTAL is that the Cl- concentration facing the intracellular aspects of these channels is a determinant of channel open time probability (Po). The K1/2 for maximal activation of Po by Cl- facing intracellular domains of these channels is 10 mM Cl-. The present experiments evaluated the nature of these Cl(-)-interactive sites. First, we found that the impermeant anion isethionate, when exposed to intracellular Cl- channel faces, could augment Po with a K1/2 in the range of 10 mM isethionate without affecting conductance (gCl, pS). Second, pretreatment of the solutions facing the intracellular aspects of the channels with either 1 mM phenylglyoxal (PGO), an arginine-specific reagent, or the lysine/terminal amine reagent trinitrobenzene sulfonic acid (TNBS, 1 mM), prevented the activation of Po usually seen when the Cl- concentration of solutions facing intracellular channel domains was raised from 2 to 50 mM. However, when the Cl- channel activity was increased by first raising the Cl- concentration bathing intracellular channel faces from 2 to 50 mM, subsequent addition of either PGO or TNBS to solutions bathing intracellular Cl- channel faces had no effect on Po. We conclude that the intracellular aspects of these Cl- channels contain Cl(-)-interactive loci (termed [Cl]i) which are accessible to impermeant anions in intracellular fluids and which contain arginine- and lysine-rich domains which can be inactivated, at low ambient Cl- or isethionate concentrations, by interactions with PGO or TNBS.

Animals↗

PubMed1991

Chloride efflux from isolated choroid plexus.

Chloride efflux was analyzed in adult rat lateral ventricle choroid plexus (LVCP) incubated in artificial CSF (aCSF) at 37 degrees C. Following steady-state loading of 36Cl in LVCP, the tracer release from plexus to aCSF was quantified by the efflux coefficient (k, s-1), equal to ln 2/t/2. Cl efflux could be described by a 2-component model, with a t/2 for the 'fast' component matching well that for [3H]sucrose (extracellular marker) and a slower, drug-inhibitable component of 36Cl release thought to reflect cellular washout. The cellular Cl efflux was more than twice as fast as 37 degrees C than at 15 degrees C. There was progressively more rapid efflux (k) of 36Cl from cells as the aCSF was altered over a range of several pH values from 6.7 (k = 0.026 s-1) to 8.2 (0.070 s-1). CSF medium anion replacement (isethionate and HEPES for Cl and HCO3, respectively) reduced the k for 36Cl by 57%. Acetazolamide (0.1 mM) and other Cl transport inhibitors (disulfonic stilbenes and loop diuretic) reduced Cl efflux by 35-55%. Acetazolamide inhibited Cl release from LVCP into aCSF whether the latter contained Cl and HCO3, or not. Overall, the findings suggest that Cl extrusion from choroid plexus is by way of an anion exchanger and via channels.

Acetazolamide↗

PubMed1997

A role for chloride in the suppressive effect of acetylcholine on afferent vestibular activity.

Afferents of the frog semicircular canal (SCC) respond to acetylcholine (ACh) application (0.3-1.0 mM) with a facilitation of their activity while frog saccular afferents respond with suppression (Guth et al., 1994). All recordings are of resting (i.e., non-stimulated) multiunit activity as previously reported (Guth et al., 1994). Substitution of 80% of external chloride (Cl-) by large, poorly permeant anions of different structures (isethionate, methanesulfonate, methylsulfate, and gluconate) reduced the suppressive effect of ACh in the frog saccular afferents. This substitution did not affect the facilitatory response of SCC afferents to ACh. Chloride channel blockers were also used to test further whether Cl- is involved in the ACh suppressive effect. These included: niflumic and flufenamic acids, picrotoxin, 5-nitro-2-(-3-phenylpropylamino)benzoic acid (NPPB), and 4,4'-dinitrostilbene-2,2'-disulfonic acid (DNDS). As with the Cl- substitutions, all of these agents reduced the suppressive response to ACh in the saccule, but not the facilitatory response seen in the SCC. The suppressive effect of ACh on saccular afferents is considered to be due to activation of a nicotinic-like receptor (Guth et al., 1994; Guth and Norris, 1996). Taking into account the effects of both Cl- substitutions and Cl- channel blockers, we conclude that changes in Cl- availability influence the suppressive effect of ACh and that therefore Cl- may be involved in this effect.

Acetylcholine↗

PubMed1985

Distribution of plasmid-borne resistance to nucleic acid binding compounds in methicillin-resistant Staphylococcus aureus.

Methicillin-resistant Staphylococcus aureus (MRSA) which are epidemic in Australian hospitals have been found to be genetically different from strains previously isolated in Australia and in Europe. A characteristic feature of the recent Australian isolates is a plasmid which encodes resistance to nucleic acid binding compounds (NAB) such as propamidine isethionate. Of 753 MRSA strains isolated from around the world in 1980-1983, c. 60% were NAB resistant. The determinant for this resistance could be transferred from 90% of strains to a recipient strain in mixed culture. A plasmid analysis revealed that, in general, the largest plasmid of MRSA isolates coded for NAB resistance and may carry other determinants for penicillinase production and resistance to gentamicin, trimethoprim, neomycin, tetracycline, cadmium and mercury. Some plasmids exhibited unusual behaviour with the appearance of deletion mutants after transfer and, in one case, a high-frequency alteration in the expression of gentamicin resistance from high-level to low-level resistance, correlated to a deletion of c. 0.5 megadalton of plasmid DNA. These results demonstrate that these NAB-resistance plasmids are not unique to Australian MRSA strains but are widely distributed throughout the world.

Benzamidines↗

PubMed1988

Stimulation of acid formation in permeable gastric glands by valinomycin.

Isolated gastric glands made permeable with digitonin treatment were employed to study the ionic requirements of acid formation. Acid formation was monitored by the accumulation of a novel weak base probe, [14C]benzylamine. ATP-dependent acid formation was found to require K+ in a concentration-dependent manner, with an apparent K0.5 = 7 mM. The anion dependence of acid formation gave a selectivity sequence of Cl = I greater than Br greater than NO3 greater than SO4 = isethionate, with isethionate being approximately 50% as effective as Cl. The dependence of acid formation on [Cl] gave an apparent K0.5 = 6 mM. Addition of the K+ ionophore, valinomycin, to resting glands (cimetidine pretreatment) resulted in a two- to threefold increase in ATP-dependent acid formation. In contrast, stimulated (forskolin pretreated) glands showed a greater accumulation of benzylamine with ATP but significantly less valinomycin stimulation. The valinomycin stimulation required both K+ and Cl- and was inhibited by omeprazole and Sch 28080. The results are interpreted to indicate that major events in the transition from a resting to a stimulated state include changes in both K+ and anion permeability of the secretory membrane of parietal cells.

Animals↗

PubMed1982

Ammonium action on post-synaptic inhibition in crayfish neurones: implications for the mechanism of chloride extrusion.

1. The reversal potential of the Cl(-)-dependent, inhibitory post-synaptic potential (E(i.p.s.p.)) was measured in the isolated crayfish stretch receptor neurone using two intracellular micro-electrodes. The difference between E(i.p.s.p.) and the resting membrane potential (E(m)), the i.p.s.p. driving force, was reversibly decreased by addition of NH(3)/NH(4) (+), and the mechanism of this decrease was investigated.2. The NH(3)/NH(4) (+)-induced decrease in i.p.s.p. driving force was dose-dependent with an onset at about 0.2 mM. E(i.p.s.p.) always remained more negative than E(m) or, when the neurone was spontaneously firing, the threshold potential. E(m) and resting membrane resistance (R(m)) also decreased in a dose-dependent fashion. Synaptic conductance (g(s)) increased with low doses, but decreased on application of 20 mM-NH(3)/NH(4) (+). All the effects were fully reversible on return to normal Ringer solution.3. Intracellular acidification (substitution of 50% Cl(-) by acetate compared with isethionate) considerably reduced the i.p.s.p. driving force. Simultaneous application of NH(3)/NH(4) (+) and acetate-substituted Ringer solution caused a similar decrease in the driving force to application of the same concentration of NH(3)/NH(4) (+) under normal conditions. Increasing the extracellular pH at which a given concentration of NH(3)/NH(4) (+) was applied caused a smaller decline in the i.p.s.p. driving force. These results suggest that intracellular acidification decreases the i.p.s.p. driving force and that the NH(3)/NH(4) (+)-induced decline is caused by an action of the ammonium ion.4. Elevation of extracellular K(+) (K(+) (0)) decreased the i.p.s.p. driving force, E(m) and R(m), and increased g(s). Reduction of K(+) (0) had the converse effects on all parameters.5. Application of Rb(+) or Cs(+) mimicked the effects of NH(3)/NH(4) (+). Substitution of K(+) (0) by Rb(+), Cs(+) or NH(3)/NH(4) (+) opposed or even reversed the increase in i.p.s.p. driving force when Na(+) was used as the substitute. The effectiveness of the various cations in decreasing the driving force was in the following order: Rb(+) > NH(4) (+) > K(+) > Cs(+).6. Inhibition of the Na pump by ouabain or K(+)-free Ringer solution caused a gradual reduction in the i.p.s.p. driving force. Since the driving force also decreased when the Na(+) gradient probably was increased (elevated K(+) (0)), this suggests a dependence on the K(+) gradient rather than the Na(+) gradient or the Na pump itself.7. Frusemide (6 x 10(-4) M) reversibly decreased the i.p.s.p. driving force and E(m), and increased g(s). R(m) was not significantly affected. Application of frusemide in the presence of 5 mM-Rb(+) and vice versa, caused a further reduction in the driving force. The recovery of the driving force on removal of either agent was slowed by the presence of the other.8. Application of 4,4-diisothiocyanostilbene-2,2-disulphonic acid (DIDS; 10(-4) M) caused spontaneous firing and reduced E(i.p.s.p.) to the threshold potential. R(m) and g(s) increased. The effects were slowly reversible on removal of the drug.9. It is proposed that the i.p.s.p. driving force is maintained by a K(+)-Cl(-) co-transport mechanism, driven by the K(+) gradient. The K(+) site exhibits the binding selectivity: Rb(+) > NH(4) (+) > K(+) > Cs(+) and the mechanism is inhibited partially by frusemide and completely by DIDS.

Acetates↗

PubMed1993

Inhibition of a neuronal voltage-dependent chloride channel by the type II pyrethroid, deltamethrin.

Following the previous finding that the Type II pyrethroid, deltamethrin, increased membrane resistance in peripheral nerve and muscle in a chloride-dependent manner, the action of deltamethrin on neuronal voltage-dependent chloride channels was assessed using inside-out patches from NIE-115 neuroblastoma cells. These were bathed in symmetrical solutions, containing 149 mM chloride and the membrane potential stepped from 0 mV to voltages ranging from +/- 10 to 80 mV for 2 or 5 sec. Active patches contained large conductance channels (343 +/- 11 pS, n = 8), which inactivated relatively slowly during the voltage step and could be resolved into a number of substates. The channels were confirmed as being chloride specific on the basis of substitution experiments with isethionate and pharmacological blockade by 9-anthracene carboxylic acid (9-ACA). Within 20 min of adding deltamethrin (2 microM) to the bath solution, open channel probability (Po) fell from 0.50 +/- 0.06 to 0.24 +/- 0.04 (n = 11) a highly significant result. Glycerinformal solvent alone (0.1% v/v) caused a non-significant rise to 0.65 +/- 0.09 (n = 4). The decreased open channel probability after deltamethrin was due to an increased incidence of both the closed channel state and low conductance substates. In addition, deltamethrin frequently caused flickering between substrates similar to that seen after 9-ACA. Deltamethrin did not change single channel conductance, current-voltage relationship or time-dependent channel inactivation, but decreased open channel probability over the complete range of membrane voltage tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1997

Calcium-activated chloride current in normal mouse sympathetic ganglion cells.

1. In rat sympathetic ganglion cells, axotomy induces the appearance of a depolarizing after-potential (ADP) produced by a calcium-activated chloride current. Here we report that this current is also present in normal sympathetic neurones from the mouse. 2. In an in vitro preparation of the superior cervical ganglion, an ADP was observed after spike firing in 50% of the cells studied with single-electrode current- and voltage-clamp techniques. 3. When the cells were voltage clamped at -50 mV in the presence of tetrodotoxin (TTX) and tetraethylammonium chloride (TEA), depolarizing jumps evoked inward calcium currents which were contaminated by outward chloride currents, followed by slowly decaying inward chloride tail currents. 4. The ADP and the inward tail currents disappeared when calcium was removed from the extracellular solution or when cadmium was added. 5. The reversal potential for the inward tail current was approximately -24 mV and was displaced in agreement with the Nernst equation for chloride when the extracellular NaCl was replaced by sucrose or sodium isethionate. The chloride channel blocker anthracene-9-carboxylic acid (9AC) inhibited both the ADP and the tail current. 6. Using intracellular injection of neurobiotin, we found that cells with shorter dendrites had larger ADPs. In axotomized ganglia practically all cells showed very pronounced ADPs. 7. We conclude that normal mouse sympathetic ganglion cells have a calcium-activated chloride current that generates an ADP. The channels responsible for this current are probably located in the dendrites.

Action Potentials↗

PubMed1988

Effect of sodium-ascorbate and vanadate on the Rb+-uptake of human red blood cells.

To follow the Rb+-uptake of human red blood cells (rbc-s) under different circumstances, a micro-method was developed. According to our experiments the Rb+-uptake of rbc-s in a healthy person was about 3.5-4.0 mumoles Rb/mg Fe at 37 degrees C during 120 minutes. When red cells were incubated with solutions containing different concentrations, between 15 and 120 mmole/l, of Na-ascorbate [Na-ascorbate was applied at the expense of Na-isethionate (sodium salt of 2-hydroxyethan-1-sulfonic acid)] the Rb+-uptake of red cells increased at 37 degrees C with 37 to 70% respectively. In other experiments it was established that the ouabain-sensitive Rb+-uptake of rbc-s decreased with 50% in the presence of 0.1 mmole/l vanadate, while if Na-ascorbate was applied simultaneously with different concentrations of vanadate, or after a preincubation with 1 mmole/l vanadate, the Rb+-uptake of red cells, which had been reduced by vanadate, returned close to that of control. This effect can be explained by the reductive property of Na-ascorbate, i.e. by the transformation of vanadate to vanadil.

Ascorbic Acid↗