lithium-chloride and rubidium-chloride

The neuro-protective effects of rubidium and lithium as alkali metals have been reported for different central nervous system dysfunctions including mania and depression. The aim of this study was evaluating as well as comparing the effects of rubidium chloride (RbCl) and lithium chloride (LiCl) on different seizures paradigms in mice and determining the involvement of NMDA receptors and nitrergic pathway. To assess the seizures threshold, animals received intravenous pentylenetetrazole (PTZ, 0.5%; 1 mL/min). Male NMRI mice (6-8 weeks) received intraperitoneal (i.p.) injections of different doses of RbCl and LiCl. Doses greater than 10 mg/kg of RbCl showed a significant anticonvulsant activity 60 min after administration; the anticonvulsant effects of LiCl was observed at the doses more than 5 mg/kg and after 30 min in PTZ-induced seizure threshold. But, RbCl (10, 20 mg/kg, i.p) or LiCl (5, 10 mg/kg, i.p) injection did not induce protection against maximal electroshock (MES) or intraperitoneal injection of PTZ lethal dose (80 mg/kg)-induced seizure models. Pre-treatment with L-NAME (non-selective nitric oxide synthase (NOS) inhibitor, 10 mg/kg; i.p.) and 7-nitroindazole (selective neuronal NOS inhibitor, 30 mg/kg; i.p.) enhanced the anticonvulsive effects of both RbCl (5 mg/kg, i.p.) and LiCl (1 mg/kg, i.p.) in PTZ-induced seizure threshold model. Injection of MK-801 (NMDA receptor antagonist, 0.05 mg/kg; i.p.) before RbCl (5 mg/kg, i.p.; P < 0.001) and LiCl (1 mg/kg, i.p.; P < 0.001) administration increased the anti-seizure activity. But, treatment with L-arginine (precursor of nitric oxide, 100 mg/kg; i.p.) decreased the seizure threshold of both RbCl (20 mg/kg, i.p.; P < 0.001) and LiCl (10 mg/kg, i.p.; P < 0.001). Measurement of nitrite levels in hippocampus of animals revealed a remarkable reduction after treatment with RbCl (20 mg/kg, i.p; P < 0.05) and LiCl (10 mg/kg, i.p; P < 0.01). To conclude, rubidium may protect central nervous system against seizures in PTZ-induced seizures threshold model through NMDA/nitrergic pathways with a similarity to lithium effects in mice.

Topics: Animals; Anticonvulsants; Chlorides; Glutamic Acid; Lithium Chloride; Male; Mice; Neuroprotective Agents; Nitric Oxide; Pentylenetetrazole; Receptors, N-Methyl-D-Aspartate; Rubidium; Seizures; Signal Transduction

We study the ion-specific salting-out process of benzene in aqueous alkali chloride solutions using Kirkwood-Buff (KB) theory of solutions and molecular dynamics simulations with different empirical force field models for the ions and benzene. Despite inaccuracies in the force fields, the simulations indicate that the decrease of the Setchenow salting-out coefficient for the series NaCl > KCl > RbCl > CsCl is determined by direct benzene-cation correlations, with the larger cations showing weak interactions with benzene. Although ion-specific aqueous solubilities of benzene may be affected by indirect ion-ion, ion-water, and water-water correlations, too, these correlations are found to be unimportant, with little to no effect on the Setchenow salting-out coefficients of the various salts. We further considered LiCl, which is experimentally known to be a weaker salting-out agent than NaCl and KCl and, therefore, ranks at an unusual position within the Hofmeister cation series. The simulations indicate that hydrated Li(+) ions can take part of the benzene hydration shell while the other cations are repelled by it. This causes weaker Li(+) exclusion around the solute and a resulting, weaker salting-out propensity of LiCl compared to that of the other salts. Removing benzene-water and benzene-salt electrostatic interactions in the simulations does not affect this mechanism, which may therefore also explain the smaller effect of LiCl, as compared to that of NaCl or KCl, on aqueous solvation and hydrophobic interaction of nonpolar molecules.

Topics: Benzene; Cations; Cesium; Chlorides; Lithium Chloride; Molecular Dynamics Simulation; Potassium Chloride; Rubidium; Sodium Chloride; Solubility; Thermodynamics; Water

The altered electrolyte handling of the choroid plexus was investigated in rats with acute renal failure (ARF) using lithium and rubidium as surrogate markers for sodium and potassium, respectively. Firstly, the transport of these two markers from the plasma to cerebrospinal fluid (CSF) was evaluated after they were concurrently injected into the femoral vein. As a result, their disposition from the plasma to CSF was shown to decrease in ARF rats, but the relationship profile between those two markers was not different from that observed in normal rats, indicating that the decreased disposition of lithium and rubidium occurs without affecting the stoichiometric balance. To clarify the mechanisms accounting for the decreased disposition, an inhibition study was then performed. When bumetanide, an inhibitor of the Na(+) /K(+) /2Cl(-) co-transporter, was directly introduced into the cerebroventricle prior to lithium and rubidium being intravenously administered, a marked increase in the markers' disposition was observed. However, such an increased disposition did not occur when bumetanide was injected into the femoral vein. Other inhibitors, such as amiloride for the Na(+) /H(+) exchanger and ouabain for Na(+) /K(+) -ATPase, did not show any effects on marker disposition regardless of the inhibitor being administered into either the cerebroventricle or femoral vein. These findings suggest that the decreased marker disposition in ARF rats is due to an increased efflux process of the choroid plexus mediated by the Na(+) /K(+) /2Cl(-) co-transporter. That is, electrolyte efflux from the CSF to plasma increases, and thereby the electrolyte influx from the plasma to CSF is counteracted.

Topics: Acute Kidney Injury; Animals; Area Under Curve; Bumetanide; Chlorides; Choroid Plexus; Electrolytes; Glycerol; Ion Transport; Lithium Chloride; Male; Potassium; Rats; Rats, Wistar; Rubidium; Sodium; Sodium-Potassium-Chloride Symporters; Solute Carrier Family 12, Member 2

The physiological role of Candida albicans Cnh1, a member of the Na+/H+ antiporter family, was characterized. Though CaCnh1p had broad substrate specificity and mediated efflux of at least four alkali metal cations upon heterologous expression in Saccharomyces cerevisiae, its presence in C. albicans cells was important especially for potassium homeostasis. In C. albicans, CaCnh1p tagged with GFP was localized in the plasma membrane of cells growing as both yeasts and hyphae. Deletion of CNH1 alleles did not affect tolerance to NaCl, LiCl or CsCl, but resulted in increased sensitivity to high external concentrations of KCl and RbCl. The potassium and rubidium tolerance of a cnh1 homozygous mutant was fully restored by reintegration of CNH1 into the genome. The higher sensitivity of the cnh1/cnh1 mutant to external KCl was caused by a lower K+ efflux from these cells. Together, the functional characterization of the CaCnh1 antiporter in C. albicans revealed that this antiporter plays a significant role in C. albicans physiology. It ensures potassium and rubidium tolerance and participates in the regulation of intracellular potassium content of C. albicans cells.

Topics: Anti-Bacterial Agents; Candida albicans; Cell Membrane; Cesium; Chlorides; Cloning, Molecular; Drug Resistance, Fungal; Fungal Proteins; Gene Deletion; Gene Expression; Genetic Complementation Test; Homeostasis; Hyphae; Lithium Chloride; Potassium; Potassium Chloride; Rubidium; Saccharomyces cerevisiae; Sodium Chloride; Sodium-Hydrogen Exchangers; Substrate Specificity; Yeasts

Ion current through single outer membrane protein F (OmpF) trimers was recorded and compared to molecular dynamics simulation. Unidirectional insertion was revealed from the asymmetry in channel conductance. Single trimer conductance showed particularly high values at low symmetrical salt solution. The conductance values of various alkali metal ion solutions were proportional to the monovalent cation mobility values in the bulk phase, LiCl

Topics: Aspartic Acid; Cation Transport Proteins; Cations, Monovalent; Cesium; Chlorides; Computational Biology; Electric Conductivity; Lipid Bilayers; Lithium Chloride; Models, Molecular; Patch-Clamp Techniques; Porins; Potassium Chloride; Rubidium; Sodium Chloride; Thermodynamics

The influence of three univalent salts (LiCl, NaCl and RbCl) on the separation of amino acids labelled with 3-(4-carboxybenzoyl)-quinoline-2-carboxaldehyde (CBQCA) in micellar capillary electrophoresis has been studied. Capacity factors for a series of eight CBQCA-labelled amino acids in a sodium dodecyl sulfate (SDS) micellar system containing different concentrations of salt were measured and were found to be related to both the hydrodynamic radius of the salt counter-ion (Li(+), Na(+), Rb(+)) and the relative hydrophobicity of the amino acid. Affinities of the analytes for the micelles were generally observed to decrease as the salt concentration in the background electrolyte was increased from 10 to 50 mM. This decrease in affinity was greatest in the presence of the salt counter-ion with the smallest hydrodynamic radius and is primarily due to an increased resistance to mass transfer. Furthermore, interaction of hydrophobic analytes with the micelles is greater than that of hydrophilic analytes at all salt concentrations due to the greater strength of the hydrophobic interactions and this effect is also enhanced in the presence of a smaller counter-ion. No negative effects due to Joule heating or electromigrative dispersion were observed for low to moderate concentrations of salt, which suggests that the use of simple univalent salts to modify analyte/micelle affinities can be a practical method for improving the separation of complex mixtures.

Topics: Amino Acids; Benzoates; Cations, Monovalent; Chlorides; Electrophoresis, Capillary; Fluorescent Dyes; Heating; Lithium Chloride; Micelles; Quinolines; Rubidium; Sodium Chloride

1. The lipid bilayer technique was used to characterize the biophysical and pharmacological properties of several ion channels formed by incorporating amyloid beta protein fragment (AbetaP) 1-40 into lipid membranes. Based on the conductance, kinetics, selectivity, and pharmacological properties, the following AbetaP[1-40]-formed ion channels have been identified: (i) The AbetaP[1-40]-formed "bursting" fast cation channel was characterized by (a) a single channel conductance of 63 pS (250/50 mM KCl cis/trans) at +140 mV. 17 pS (250/50 mM KCl cis/trans) at -160 mV, and the nonlinear current-voltage relationship drawn to a third-order polynomial, (b) selectivity sequence PK > PNa > PLi = 1.0:0.60:0.47, (c) Po of 0.22 at 0 mV and 0.55 at +120 mV, and (d) Zn2+-induced reduction in current amplitude, a typical property of a slow block mechanism. (ii) The AbetaP[1-40]-formed "spiky" fast cation channel was characterized by (a) a similar kinetics to the "bursting" fast channel with exception for the absence of the long intraburst closures, (b) single channel conductance of 63 pS (250/50 KCl) at +140 mV 17 pS (250/50 KCl) at -160 mV, the current-voltage relationship nonlinear drawn to a third-order polynomial fit, and (c) selectivity sequence PRb > (iii) The AbetaP[1-40]-formed medium conductance channel was charcterized by (a) 275 pS (250/50 mM KCl cis/trans) at +140 mV and 19 pS (250/50 mM KCl cis/trans) at -160 mV and (b) inactivation at Vms more negative than -120 and more positive than +120 mV. (iv) The AbetaP[1-40]-formed inactivating large conductance channel was characterized by (a) fast and slow modes of opening to seven multilevel conductances ranging between 0-589 pS (in 250/50 mM KCI) at +140 mV and 0-704 pS (in 250/50 mM KCl) at -160 mV. (b) The fast mode which had a conductance of <250 pS was voltage dependent. The inactivation was described by a bell-shaped curve with a peak lag time of 7.2 s at +36 mV. The slow mode which had a conductance of >250 pS was also voltage dependent. The inactivation was described by a bell-shaped curve with a peak lag time of 7.0 s at -76 mV, (c) the value of PK/Pcholine for the fast mode was 3.9 and selectivity sequence PK > PCs > PNa > PLi = 1.0:0.94:0.87:0.59. The value of PK/Pcholine for the slow mode was 2.7 and selectivity sequence PK > FNa > PLi > PCs = 1.0:0.59:0.49:0.21, and (d) asymmetric blockade with 10 mM Zn2+-induced reduction in the large conductance state of the slow mode mediated via slow block mechani

Topics: Alzheimer Disease; Amyloid beta-Peptides; Cations; Cesium; Chlorides; Humans; Ion Channel Gating; Ion Channels; Kinetics; Lipid Bilayers; Lithium Chloride; Membrane Potentials; Patch-Clamp Techniques; Peptide Fragments; Potassium Chloride; Rubidium; Signal Transduction; Sodium Chloride; Structure-Activity Relationship; Zinc Compounds

Rubidium and lithium are alkali metals belonging to the same periodic series as sodium, potassium and cesium. In the present report the effects of lithium and rubidium on animal reactivity to stressful stimuli and on dopamine output in the nucleus accumbens were studied. A dose-response curve with rubidium, administered acutely before exposure to unavoidable stress, showed a maximal protective activity on escape deficit development at the dose of 0. 41 mEq/kg. Rubidium injected at doses of 0.008-0.08 mEq/kg 72 h before the unavoidable stress had the same efficacy as the acute 0. 41 mEq/kg dose. Tolerance to the effect of rubidium developed after 9 days of treatment and, on day 15, rats presented a spontaneous escape deficit. The acute effect of lithium, administered for 3.5 days at the dose of 0.8 mEq/kg, i.p. twice a day before the exposure to unavoidable stress, was analogous to that of rubidium, but after repeated treatment a spontaneous escape deficit developed. Rats showing an escape deficit secondary to chronic stress also presented decreased extraneuronal dopamine concentrations in the nucleus accumbens. Accordingly, microdialysis studies showed significantly lower extracellular dopamine levels in rats chronically treated with lithium or rubidium compared to control animals. Cocaine (5 mg/kg i. p.) administered acutely increased extracellular dopamine concentrations in control rats, as well as in rats chronically stressed or chronically treated with lithium or rubidium. However, the dopamine increase was significantly higher in controls compared to the other groups. In conclusion, long-term treatment with lithium or rubidium, or the exposure to chronic stress, produced a condition of behavioral hypo-reactivity accompanied by a decreased dopamine output in the nucleus accumbens.

Topics: Animals; Antimanic Agents; Brain Chemistry; Chlorides; Chronic Disease; Cocaine; Dopamine; Dopamine Uptake Inhibitors; Escape Reaction; Lithium Chloride; Male; Microdialysis; Neurons; Nucleus Accumbens; Rats; Rats, Sprague-Dawley; Rubidium; Stress, Physiological

The effects of different doses of lithium (5-320 mg/kg intramuscularly) and rubidium (0.25 32 mg/kg intramuscularly) on apomorphine-induced pecking were investigated in pigeons. These two cations did not induce pecking by itself. Intramuscular administration of apomorphine (a mixed D1/D2 dopamine receptors agonist, 0.1-1.6 mg/kg) induced pecking in a dose-dependent manner. SCH 23390 (D1 dopamine receptor antagonist, 0.02-0.08 mg/kg) and sulpiride (D2 dopamine receptor antagonist, 25-100 mg/kg) decreased apomorphine-induced pecking dose-dependently. Combination of SCH 23390 (0.04 mg/kg) with sulpiride (50 mg/kg) caused a stronger inhibitory effect on apomorphine response. This indicates that both D1 and D2 dopamine receptors are involved in apomorphine-induced pecking. The response induced by apomorphine (0.2-0.8 mg/kg) was decreased in animals pretreated with lithium and rubidium. In these conditions, SCH 23390 and sulpiride produced a larger inhibitory effect on the apomorphine response, suggesting that acute lithium and rubidium pretreatment inhibit pecking by interfering with dopaminergic mechanisms.

Topics: Animals; Apomorphine; Chlorides; Columbidae; Dopamine Agonists; Lithium Chloride; Rubidium; Stereotyped Behavior

Lithium, a monovalent cation, is the mainstay in the treatment of manic-depressive (MDI) illness, but despite extensive research, its mechanism of action remains to be elucidated. Since lithium requires chronic administration for therapeutic efficacy, and because its beneficial effects last well beyond its discontinuation, it has been postulated that lithium may exert major effects at the genomic level. In the present study we found that lithium, at therapeutically relevant concentrations, increases AP-1 DNA binding activity in human SH-SY5Y cells and rat C6 glioma cells. Additionally, in both SY5Y and C6 cells transiently transfected with a reporter gene vector driven by an SV40 promoter, lithium increased the activity of the reporter gene in a time- and concentration-dependent manner. Furthermore, mutations in the AP-1 sites of the reporter gene promoter significantly attenuated lithium's effects. These data indicate that lithium stimulates gene expression through the AP-1 transcription factor pathway, effects which may play a role in its long-term mood-stabilizing effects.

Topics: Animals; Base Sequence; Binding Sites; Chlorides; Consensus Sequence; Gene Expression Regulation, Neoplastic; Genes, Reporter; Glioma; Humans; Lithium Chloride; Luciferases; Molecular Sequence Data; Mutagenesis, Site-Directed; Neuroblastoma; Potassium Chloride; Promoter Regions, Genetic; Rats; Recombinant Fusion Proteins; Rubidium; Sequence Alignment; Sequence Homology, Nucleic Acid; Simian virus 40; Transcription Factor AP-1; Transfection; Tumor Cells, Cultured

N-acetyl-beta-D-glucosaminidase (NAG) is one of the sensitive hydrolytic lysosomal enzymes which is released after renal tubular damages. We studied gentamicin-induced nephrotoxicity by determining the NAG release in perfused rat kidney. 100 micrograms/ml of gentamicin caused a time-dependent increase in enzymuria, peaking at 90 min. At this time the released NAG is about sixfold more than the control. The effect of concurrent perfusion with 100 micrograms/ml gentamicin and with 0.5 mmol/l lithium chloride or 0.5 mmol/l rubidium chloride in the perfusion fluid was also studied by measuring NAG activity in the perfusate. Both cations decrease the gentamicin-induced NAG release. However, the inhibitory effect of lithium chloride may be due to interference of this ion with the polyphosphoinositide cycle in renal tubular lysosomal membranes. There is no obvious evidence for an inhibitory effect of rubidium chloride.

Topics: Acetylglucosaminidase; Analysis of Variance; Animals; Chlorides; Dose-Response Relationship, Drug; Enzyme Inhibitors; Gentamicins; Hydrogen-Ion Concentration; Kidney; Kidney Tubules; Lithium Chloride; Lysosomes; Male; Perfusion; Phosphatidylinositol Phosphates; Rats; Rats, Sprague-Dawley; Rubidium

Previous studies have suggested a causal connection between abnormalities of the circadian system and affective disorders. The effectiveness of lithium or rubidium as a treatment for affective disorders and the ability of lithium or rubidium to influence circadian pacemakers has stimulated research into the mechanism of lithium's action on circadian systems. In this study we used a neuronal in vitro circadian pacemaker preparation, the eye of the mollusc Bulla, to examine the cellular effects of lithium and rubidium. Continuous extracellular LiCl application lengthens the period of the circadian rhythm of the Bulla pacemaker in a concentration-dependent manner. Rubidium was found to be more effective than lithium in period lengthening. Stable phase delays were generated by 2-h pulses of 395 mM LiCl applied extracellularly from zeitgeber time (ZT) 5-7 (mid subjective day). Concomitant continuous application of 16 mM LiCl and light (a depolarizing agent) generated period lengthening substantially greater than the arithmetic sum of the modest period lengthening of each treatment alone. Furthermore, LiCl pulses, applied together with depolarizing extracellular KCl concentrations, yielded an increasing magnitude of phase delays with increasing KCl concentration. These data suggest that LiCl acts intracellularly on the circadian pacemaker cells by entering through a voltage-dependent channel, most likely a sodium channel.

Topics: Animals; Chlorides; Circadian Rhythm; Darkness; Light; Lithium Chloride; Mollusca; Neurons; Optic Nerve; Potassium Chloride; Rubidium; Time

Stimulation of the frog tongue with various salts produced changes in epithelial potential of the tongue, accompanied by changes in gustatory nerve activity. Both changes varied similarly according to the stimulus. The results indicate that cation transport in the lingual epithelium is involved in gustation.

Topics: Animals; Biological Transport; Chlorides; Choline; Epithelium; Glossopharyngeal Nerve; Lithium; Lithium Chloride; Membrane Potentials; Potassium Chloride; Rana catesbeiana; Rubidium; Sodium Chloride; Sulfuric Acid Esters; Taste; Tongue

Cation fluxes and intracellular content in mouse fibroblasts L, growing for more than three years in the Dulbecco modified Eagle's serum-free medium (clone L625sf) were measured as a function of culture density. The cells show no density-dependent inhibition of growth and in continuously growing cultures of L625sf cells internal potassium, and rubidium influx was found to remain high within a wide range of densities (5.10(4)-20.10(4) cells/cm2). A close correlation was revealed between the potassium transport and the proliferative state of L625sf cultures: the addition of 5% calf serum to logarithmically growing cultures leads to the increase in culture growth rate as well as to the increase in ouabain-inhibited rubidium influx and intracellular potassium content; a delay in culture growth rate due to medium depletion is accompanied by decreasing both the rubidium influx and the intracellular potassium content. It is concluded that L625sf cells being capable of multiplicating in serum-free medium remain sensitive to growth factors of serum and may be used for study of growth factor induction of cell proliferation and for identification of autocrine factors of cell growth.

Topics: Animals; Biological Transport; Cations; Cell Division; Chlorides; Culture Media; L Cells; Lithium; Lithium Chloride; Mice; Ouabain; Potassium; Rubidium; Sodium; Time Factors

Lithium chloride and rubidium chloride were tested under conditions in which the effects of their chronic administration on aversively-controlled behavior could be assessed. Lithium attenuated shock-induced suppression of open-field activity when that suppression was under the control of mild or moderate stimulus parameters, but had no effect on the suppression produced by the presence of shock itself. Rubidium, on the other hand, increased shock-induced suppression under all conditions. When shock was removed and extinction of the activity suppression was investigated, lithium subjects failed to return to their original baseline activity levels, while subjects receiving rubidium recovered baselines in a manner indistinguishable from that observed in control animals.

Topics: Animals; Avoidance Learning; Bipolar Disorder; Chlorides; Electroshock; Extinction, Psychological; Lithium; Lithium Chloride; Male; Models, Biological; Motor Activity; Rats; Rubidium

Rubidium and lithium influxes as well as intracellular potassium and sodium contents were investigated in L cells during the culture growth. In sparse culture over the cell densities 0.5-3 X 10(4) cells/cm2 ouabain-sensitive rubidium influx is small and ouabain-resistant lithium influx in high. With the increase in culture density up to 4-5 X 10(4) cells/cm2 the active rubidium influx, mediated by ouabain-sensitive component, is enhanced, and ion "leakage" tested by lithium influx is diminished. Simultaneously with the exponential growth of culture the intracellular potassium content is increased and the intracellular sodium content is decreased resulting in the higher K/Na ratio in cell. During the further transition to dense culture and in stationary state (10-17 X 10(4) cells/cm2) the sodium content and lithium influx do not change significantly, but the potassium content is decreased. The decrease in intracellular potassium is correlated with that in the portion of cells in S-phase from 27-30 to 12%. Thus, in transformed cells the density-dependent alterations in membrane cation transport are observed.

Topics: Animals; Biological Transport; Biological Transport, Active; Cell Count; Cell Membrane; Chlorides; Ion Channels; L Cells; Lithium; Lithium Chloride; Mice; Ouabain; Potassium; Rubidium; Sodium; Time Factors

Midbrain raphe lesions in rats (raphe rats) induce aggressive behavior including muricide. A single administration of LiCl (Li) 100 mg/kg to raphe rats produced only 25% of muricide inhibition. However, the inhibitory effect of muricide in raphe rats significantly increased from the 5th day following repeated administration of Li. Chronic Li also inhibited muricide in olfactory bulbectomized (OB) rats. The inhibition of muricide lasted until the next day to some extent. In this point, the effect of Li on muricide is similar to that of antidepressants, but not of neuroleptics. On the contrary, RbCl (Rb) showed a tendency to induce muricide. The single re-administration of Li 100 mg/kg on the withdrawal on the 7th day after repeated administration for 14 days showed a significant inhibition of muricide in raphe rats, unlike that in OB rats. Li also showed a partial prophylactic effect on muricide when Li 100 mg/kg was administered for 1 week before raphe lesions. These results suggest that raphe rats may serve not only as an experimental model of depression, but also as that of manic illness.

Topics: Aggression; Animals; Chlorides; Humans; Lithium; Lithium Chloride; Male; Olfactory Bulb; Raphe Nuclei; Rats; Rats, Inbred Strains; Rubidium; Time Factors

Methodologic and kinetic properties of gamma-aminobutyric acid (GABA) binding were studied in platelet materials of different nature. Platelet GABA binding was saturable and specific. LiCl and RbCl added in vitro at concentration of 0.01 mM increased significantly platelet GABA binding. This activator effect, and its kinetic characteristics were different from those obtained for GABA uptake and 5-hydroxytryptamine (5-HT) binding, which suggest that the three processes are different in platelets.

Topics: Adult; Binding Sites; Blood Platelets; Chlorides; Female; gamma-Aminobutyric Acid; Humans; Kinetics; Lithium; Lithium Chloride; Male; Middle Aged; Receptors, Cell Surface; Receptors, GABA-A; Rubidium; Serotonin

The methodologic and kinetic characteristics of GABA uptake by platelets were determined in blood platelets of volunteer donors. Extrapolation of a reciprocal plot indicate two uptake systems: a high affinity and a passive diffusion mechanism. When LiCl and RbCl were added in vitro, they had no effect on platelet GABA uptake. Our data suggest that platelet GABA and 5-HT uptake are carried out by different systems.

Topics: Adult; Biological Transport, Active; Blood Platelets; Chlorides; Diffusion; Female; gamma-Aminobutyric Acid; Humans; Kinetics; Lithium; Lithium Chloride; Male; Middle Aged; Rubidium; Serotonin