Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Barium Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1996

Direct measurement of ion distributions between lipid membranes with X-ray diffraction.

A new and simple method is introduced, which allows the direct measurement of the distribution of ions between lipid membranes with a conventional X-ray source. It is based on a difference method which is combined with a swelling experiment. The presented method is applied to unoriented powder samples of 1,2-dipalmitoyl-sn-glycero-3-phosphorylglycerol in different ionic solutions of RbCl and BaCl2. From these samples, results for the cation distributions with a resolution of 12 A degrees were obtained. Analysis of the experimentally obtained distributions shows that the simple Gouy-Chapman theory is probably not able to describe the experimental data consistently. Instead a better correspondence between experiment and theory is obtained with a generalized linear Gouy-Chapman model which takes into account the finite width of the lipid/electrolyte interface. Possible future improvements of the presented method with regard to the obtained resolution and the possibility to obtain ion densities on an absolute scale are discussed.

Barium Compounds↗
PubMed1990

Voltage-dependent calcium currents in trigeminal chick neurons.

The presence of action potentials, when sodium and potassium currents were blocked, has been investigated in trigeminal ganglion neurons, using the patch-clamp technique. In this conditions, inward currents, sensitive to the external application of cadmium, were detected. Activation and inactivation properties were investigated, as well as the behaviour of the current in the presence of extracellular Barium. The properties of these inward currents in trigeminal neurons are correlated to high threshold voltage-dependent calcium channels.

Action Potentials↗
PubMed1981

Control of the variability of the afferent discharge rate in frog muscle spindle by potassium blockers.

Blockage of the K+ channels in the sensory terminal of frog muscle spindle by the combined application of BaCl2 and other K+ blockers makes it possible to reversibly change the sustained and irregular discharges into non-sustained regular discharges. As a similar change in the discharge pattern is also made by application of CoCl2 alone, though it is irreversible, the irregular and sustained discharge may be due to [Ca2+]i-activated potassium conductance.

Afferent Pathways↗
PubMed1987

Maitotoxin-induced membrane current in neuroblastoma cells.

Maitotoxin (MTX) is a potent marine toxin isolated from the toxic dinoflagellate, Gambierdiscus toxicus. We have examined the possibility of MTX activating calcium channels using cultured neuroblastoma cells (N1E-115). MTX (10 ng/ml) produced a depolarization of the membrane, which was prevented by the removal of Ca2+ from the external medium. Under voltage clamp conditions, membrane currents were recorded with 50 mM Ba2+ as a charge carrier through calcium channels. After application of MTX (1 ng/ml), an inward current necessary to hold the membrane at -90 mV increased progressively. This was followed by a gradual decrease of the transient inward Ba2+ current through type I calcium channels recorded at -30 mV which was eventually abolished. A similar tendency was observed in the long-lasting inward Ba2+ current through type II calcium channels, which was recorded at +10 mV. The MTX action was antagonized by calcium channel blockers such as verapamil (100 microM) and La3+ (1 mM). A high concentration of verapamil (500 microM) blocked both types of calcium channels persistently. After washout of verapamil but while the calcium channels were still blocked, MTX (1 ng/ml) induced a steady-state current. The MTX-induced current showed an inward-rectifying property with a reversal potential of approximately -30 mV. The results suggest that the MTX-induced current does not flow through calcium channels. Thus, MTX may create a pore in the membrane with pharmacological properties similar to those of calcium channels.

Animals↗
PubMed1988

Effects of cyclic nucleotides and calcium on transduction and encoding processes in frog muscle spindle.

In decapsulated muscle spindles, application of dibutyryl cyclic AMP (d-cAMP, 0.1-10 mM) and forskolin (10-100 microM) increased the rate of spontaneous discharges and decreased the responsiveness to stretch. Addition of 2-5 mM CaCl2 or 0.5-2 mM BaCl2 to the above drugs prevented the deterioration of the responsiveness to stretch and the increase in the rate of spontaneous discharges. Similar changes in the afferent discharges were observed with application of isobutylmethyl-xanthine (IBMX, 0.5-2 mM) or carbonyl cyanide chlorophenylhydrazone (CCCP, 1-10 microM). Application of 0.1-1 mM quercetin resulted in a prolonged increase in the discharge rate, lasting 15-20 s after the release of stretch. These results suggest that cAMP is involved in the regulation of the sensory processes through a modification of intracellular calcium activity.

1-Methyl-3-isobutylxanthine↗
PubMed1991

K+ efflux pathways and neurotransmitter release associated to hippocampal ischemia: effects of glucose and of K+ channel blockers.

Ischemia of hippocampal slices leads to 86Rb+ efflux and to amino acid neurotransmitter release. This 86Rb+ efflux which corresponds to the massive K+ efflux from neuronal cells observed in ischemic animals is inhibited by glucose (IC50 = 1.7 mM). Glucose also inhibits the ischemia induced liberation of GABA and aspartate. 86Rb+ efflux is insensitive to any type of known blockers for ATP-sensitive, Ca2(+)-sensitive and voltage-sensitive K+ channels.

4-Aminopyridine↗
PubMed1991

Long-lasting decrease in the crayfish giant motoneuron soma excitability induced by Ca2+ influx.

After a single Ca-dependent action-potential or a 300 ms clamp pulse to 0 mV in the motor giant somata of the crayfish abdominal nerve cord, a decrease in input resistance, an afterhyperpolarisation and a shortening of the test action potentials were observed during 10-15 min. These effects were due to a novel type of long-lasting outward current, triggered by a single influx of Ca2+, resistant to TEA+ and blocked by Ba2+.

Action Potentials↗
PubMed1991

Potassium channel-dependent changes in the volume of developing mouse Schwann cells.

Physiological roles of voltage-gated K+ channels in developing mouse Schwann cells were investigated using whole-cell variation of the patch-clamp technique. In neonatal myelin-associated Schwann cells, local cytoplasmic swellings were induced when membrane potential (MP) was kept more negative than zero-current potential (membrane hyperpolarization) and they decreased in sizes when MP was kept positive. A lack of changes of cytoplasmic volume in Schwann cells of 17- to 18-day-old embryos or in neonatal myelin-associated cells in a solution containing Ba2+ suggested that activation of Ba(2+)-sensitive K+ channels caused cytoplasmic volume changes. Significant increase in magnitudes of Ba(2+)-sensitive K+ currents in neonatal myelin-associated cells after membrane hyperpolarization suggested that these K+ channels locate in adaxonal Schwann cell membrane and probably determine the sites of Schmidt-Lanterman incisures.

Aging↗
PubMed1993

4-Aminopyridine reduces chorda tympani nerve taste responses to potassium and alkali salts in rat.

To study the potential role of potassium channels in the taste response to potassium salts, we applied 4-aminopyridine (4-AP) to the anterior rat tongue and recorded chorda tympani nerve taste responses to chemical stimuli. 4-aminopyridine is a pharmacological blocker that reduces potassium conductance through potassium channels in nerve and muscle. Summated neural responses to stimuli dissolved in water and in 4-AP were compared. Chemical stimuli included concentration ranges of KCl, KBr, KH2PO4, CsCl, RbCl, NH4Cl, NaCl and sucrose. The blocker reduced chorda tympani responses to KCl and other potassium salts, from 0.025 to 0.25 M. Responses to ammonium, rubidium and cesium salts also were reduced, in order of effectiveness that would be predicted from known ion selectivity properties of potassium channels. Responses to NaCl and sucrose were not reduced. Other channel blockers, including tetraethylammonium chloride (TEA), BaCl2 and quinidine, did not reduce the response to KCl. These are the first detailed reports of effects of potassium channel blockers on the peripheral, neural taste response. The results are consistent with a role for potassium channels in apical taste bud cell membranes in transduction for potassium salts.

4-Aminopyridine↗
PubMed1994

Potassium and calcium channel dependence of bursting in cultured neuronal networks.

Increases in extracellular potassium concentrations reliably increase burst rates in cultured fetal murine spinal cord networks. This effect could be mimicked by either blocking voltage-gated potassium conductances or facilitating excitatory synaptic interactions, but not by blocking specific calcium-dependent potassium conductances or tonic depolarization. Spontaneous bursting in cultured networks is apparently dependent on potassium currents and intracellular calcium levels, but not on the pharmacologically characterized calcium-dependent potassium conductances.

4-Aminopyridine↗
PubMed1994

Amyloid beta-peptide (A beta P) potentiates a nimodipine-sensitive L-type barium conductance in N1E-115 neuroblastoma cells.

The neurodegenerative pathology observed in Alzheimer's Disease (AD) has been partially attributed to the neurotoxic effects of the amyloid beta-peptide (A beta P), although the mechanisms underlying this neurotoxicity are unknown. Since A beta P is capable of forming cation channels in lipid bilayers, it is possible that the neurotoxic effects on neurons may be mediated by a cation flux. We have used patch-clamp recording techniques to study the effects of A beta P on cation currents in differentiated mouse N1E-115 neuroblastoma cells. In whole-cell recordings, incubation of cells with A beta P for 24 h significantly increased the median peak inward current from -201.8 pA to -352.0 pA, and shifted the voltage at peak current (Vpeak) and that of current activation (Vact) towards more positive potentials. For untreated cells, median Vpeak was 1.7 mV and Vact was -28.9 mV, vs. 10.5 mV and -24.7 mV in A beta P-treated cells. Incubation with the reverse sequence A beta P(40-1) or A beta P(25-35) did not produce significant changes in the amplitude or kinetic behavior of the inward current. At the single channel level, A beta P added to the pipette increased the open probability of cation-conducting ion channels. As determined by cell viability counts, both A beta P(1-40) and the A beta P(25-35) fragment had neurotoxic effects; within 24 h, addition of A beta P reduced the number of viable cells by more than 50%. It is suggested that the neurotoxic effects of A beta P may be mediated by its ability to form cation channels de novo and/or alter the activity of cation channels already present in the cell membrane.

Alzheimer Disease↗
PubMed1989

Alkylation of cyclomalto-oligosaccharides (cyclodextrins) with dialkyl sulfate-barium hydroxide: heterogeneity of products and the marked effect of the size of the macrocycle.

The alkylation of cyclomalto-oligosaccharides (cyclodextrins, CDs) with dialkyl sulfate-barium hydroxide has been claimed to yield 2,6-di-O-alkyl derivatives. Re-investigation by plasma desorption-m.s. of the products of laboratory methylation of alpha CD, beta CD, or gamma CD and ethylation of beta CD and several commercial preparations revealed them to be mixtures with broad and roughly symmetrical distributions of the degree of substitution. Recrystallization separated the components only partially. Analysis of the product of methylation of a mixture of CDs established the order of reactivity gamma much greater than alpha greater than or equal to beta. The reactivity of gamma CD thus resembles that of amylose.

Alkylation↗
PubMed1982

An index for comparing the inhibitory action of vasodilators.

An index for comparing the inhibitory effects of vasodilators was developed to gain insight into their mechanism of action on vascular smooth muscle. Rat aortic strips were bathed in Krebs bicarbonate solution and were initially contracted to a stable tension by either phenylephrine or barium chloride. A vasodilator was then added and the remaining tension was noted; this was repeated for cumulative concentrations of vasodilator. At each concentration of vasodilator, the percent reduction in phenylephrine-induced tension (Phe) was compared to the percent reduction in barium-induced tension (Ba) and was expressed as a ratio (Phe/Ba). This ratio clearly separated verapamil and nifedipine (ratio less than 1), which block calcium influx, from papaverine (ratio = 1) which promotes calcium sequestration regardless of the source of calcium, and from dantrolene (ratio greater than 1) which interferes with intracellular calcium mobilization. This index provides a method for comparing the action of those agents presently classified as non-receptor specific vasodilators which act directly on vascular smooth muscle.

Animals↗
PubMed1984

Protective effects of Na salicylate against digoxin- and BaCl2-induced arrhythmias in guinea-pigs.

In pentobarbital-anaesthetized (60 mg/kg i.p.) guinea-pigs injections of Na salicylate (50 and 100 mg/kg i.v.) had a protective effect against arrhythmias induced by digoxin or BaCl2. A lower (25 mg/kg) and a higher (200 mg/kg) dose exerted no clearcut antiarrhythmic effect. Plasma concentrations of Na salicylate up to 1 mg/ml influenced neither the heart rate nor the ECG parameters. The antiarrhythmic effect of the drug may be explained by an inhibition of cardiac cyclooxygenase.

Animals↗
PubMed1987

Adenosine 5'-triphosphate release evoked by electrical nerve stimulation from the guinea-pig gallbladder.

The endogenous release of adenosine 5'-triphosphate (ATP) from strips of guinea-pig gallbladder during transmural stimulation (TS) was measured with a firefly luciferine-luciferase reaction. TS (15V, 1 ms, 0.5-5 Hz, for 1 min) caused a rapid and marked increase of ATP release in a frequency-dependent manner. Both ATP release and contractions evoked by TS (15 V, 5 Hz, 1 ms) were completely abolished in Ca-free medium. BaCl2 (3 X 10(-3) M), a direct muscle stimulant, produced almost the same degree of contractile tension as TS (15 V, 5 Hz, 1 ms) while the ATP release induced by BaCl2 was significantly reduced to about 60 percent of that induced by TS. Atropine (10(-6) M) significantly reduced TS-evoked contraction without affecting ATP release. It was suggested, therefore, that some of the ATP release induced by TS was of neural origin. Theophylline (a P1-purinoreceptor antagonist) 10(-6) M, quinidine (a non-specific P2-purinoreceptor antagonist) 10(-6) M and apamin (a potassium channel blocking agent) 10(-8) M had no effects on TS-evoked contraction and ATP release, suggesting the absence of a presynaptic autoregulatory mechanism of ATP release in the guinea-pig gallbladder.

Adenosine Triphosphate↗
PubMed1990

Use- and frequency-dependent blockade by UL-FS 49 of the if pacemaker current in sheep cardiac Purkinje fibres.

The mechanism by which the bradycardiac agent UL-FS 49 blocks the if pacemaker current was investigated in sheep Purkinje fibres using the two microelectrode voltage-clamp technique. If was activated by 1 s pulses applied between -30 mV and -120 mV at 0.4 Hz in a modified Tyrode solution containing BaCl2 and MnCl2, and with TRIS replacing most of the Na+. UL-FS 49 caused an exponential decline of the if current amplitude during a train of pulses. Both the rate and extent of the if reduction increased with drug concentration, without there being a resting blockade. Recovery from blockade followed a single exponential time course during prolonged hyperpolarizations. The recovery rate was extremely slow and increased with more negative voltages, as did the extent of steady state recovery from blockade. A frequency-dependent reduction of the diastolic depolarization rate resulted from a use-dependent blockade of the pacemaker current.

Animals↗
PubMed1992

Increased density of alpha-adrenoceptors in vas deferens of spontaneously hypertensive rats (SHR), indicated by functional and receptor binding studies.

Pharmacological parameters were determined from contractile responses mediated by alpha-adrenoceptors in vas deferens from spontaneously hypertensive rats (SHR) and corresponding normotensive controls, Wistar Kyoto rats (WKY), and compared with data obtained from radioligand binding assays. Contractile responses induced in longitudinal and circular muscle layers by the alpha-adrenoceptor agonist noradrenaline (NA) and by barium chloride were recorded as described previously. In both muscle layers the maximal effects induced by NA, but not by BaCl2, were significantly greater in SHR. As a consequence, the relative responsiveness ratio (rho) for the alpha-adrenoceptor was also larger for SHR than for WKY. NA-induced contractions of both muscle layers were competitively antagonized by indoramine. The pA2 values for indoramine and pD2 values for NA were the same in SHR and WKY, indicating that alpha-adrenoceptor affinity was not changed in SHR. Additionally, binding studies with the alpha-adrenoceptor ligand [3H]WB4101 revealed that Bmax values were greater in the vas deferens of SHR, whereas Kd values were not significantly different from those of WKY controls. In summary, although differences could not be detected for affinity-related parameters, a greater density of alpha-adrenoceptors was shown for SHR in receptor binding studies and this was corroborated by functional studies.

Animals↗
PubMed1994

Staurosporine-induced reduction of secretory function in cultured bovine adrenal chromaffin cells.

Staurosporine, a potent inhibitor of protein kinases, has been used to investigate the involvement of protein kinases in cellular processes such as secretory function and differentiation. We have been examining the effects of staurosporine on secretory function under the same conditions it induces dramatic changes in cell morphology in cultured bovine adrenal chromaffin cells. Our results show that treatment with 100 nM staurosporine reduces catecholamine release stimulated by 56 mM KCl, 10 microM nicotine, and 2 mM BaCl2 in a time-dependent manner (t1/2s, 42, 32, and 31 min, respectively). However, we demonstrate that the time-dependent effects on secretory function are not the direct result of staurosporine-induced changes in cell morphology. The effects of staurosporine on secretion stimulated by KCl, nicotine, and BaCl2 are concentration-dependent (IC50s, 6.3, 29.3, and 34.9 nM, respectively). Staurosporine pretreatment does not inhibit activated 45Ca2+ influx, but does reduce catecholamine release stimulated directly by Ca2+ from permeabilized cells. Furthermore, staurosporine also inhibits basal release with time- and concentration-dependencies (IC50, 9.3 nM and t1/2, 21 min) similar to those found for stimulated release. These results suggest that prolonged staurosporine pretreatment may result in the depletion/alteration of a component essential for the more terminal steps of the secretory process.

Adrenal Medulla↗