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Y Landry

Publications and source records attributed to Y Landry.

At least 91 records · Page 5Linked to original sources
PubMed1986

Muscarinic acetylcholine receptor: thermodynamic analysis of the interaction of agonists and antagonists.

The thermodynamic parameters of the interaction of agonists and antagonists with heart and brain muscarinic receptors were determined. The binding of quinuclidinyl [3H]benzilate and the inhibition of quinuclidinyl benzilate (QNB) binding by agonists and antagonists were examined at temperatures between 2 degrees C and 27 degrees C. The density of specific binding sites and the relative proportions of high- and low-affinity binding components of drugs were unaffected by the temperature changes. The binding of atropine was entropy driven in brain and heart membranes. In contrast, net values of these thermodynamic parameters for QNB binding and for the high-affinity binding component of pirenzepine to brain membranes were decreased with the enhancement of the temperature. The low-affinity binding component of the agonists carbachol, oxotremorine and pilocarpine was enthalpy driven. Their high-affinity binding component was entropy driven at 2 degrees C and became enthalpy driven when the incubation temperature was increased. The guanine nucleotide Gpp[NH]p partly prevented the temperature-dependent decrease of net entropy and enthalpy values. Considering that the net changes of thermodynamic parameters are relevant of the interactions between the ligand, the receptor protein and the adjoining membranous molecules, a three-state conformational model is proposed for the muscarinic receptor protein. The receptor selectivity is reappreciated owing to these three states of the receptor protein and the different components of the muscarinic receptor complexes.

Animals↗
PubMed1986

A fluorescent hydrophobic probe used for monitoring the kinetics of exocytosis phenomena.

A fluorescence method is presented for quantitatively analyzing exocytosis phenomena and monitoring their kinetics. The method is based on the particular properties of a hydrophobic fluorescent probe, 1-[4-(trimethylammonio)phenyl]-6-phenylhexa-1,3,5-triene (TMA-DPH) [Prendergast, F.G., Haugland, R.P., & Callahan, P.J. (1981) Biochemistry 20, 7333-7338; Kuhry, J.G., Fonteneau, P., Duportail, G., Maechling, C., & Laustriat, G. (1983) Cell Biophys. 5, 129-140; Kuhry, J.G., Duportail, G., Bronner, C., & Laustriat, G. (1985) Biochim. Biophys. Acta 845, 60-67]. When this probe is interacted with intact resting cells in aqueous suspensions, it labels solely the membranes that are in contact with the external medium and is incorporated into them according to a partition equilibrium; i.e., the amount of the probe incorporated is proportional to the available membrane surface. TMA-DPH is highly fluorescent in membranes and not at all in water. Thus, a measurement of the TMA-DPH fluorescence intensity provides a signal proportional to the membrane surface. In secretory cells, the membrane surface available for the probe is increased upon fusion of the membrane of the secretory granules with the cell plasma membranes, directly or via intergranule fusion. Thus, when these cells are stimulated, more TMA-DPH is incorporated than in resting cells since the probe is allowed to also interact with the granule membranes now connected with the external medium by pores. This process results in a proportional increase in the TMA-DPH fluorescence intensity. The response was found to be very rapid and able to follow accurately the exocytosis kinetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Labelling of the inner side of granules membrane during exocytosis. A method to differentiate secretion processes.

A fluorescence method to monitor quantitatively exocytosis phenomena in suspensions of intact cells was investigated, on the basis of the particular incorporation properties of a specific plasma membrane fluorescent label trimethylammonium-diphenylhexatriene (TMA-DPH). The method was tested with purified peritoneal mast cells stimulated by compound 48/80. Kinetics and dose-dependent response to compound 48/80 could be described accurately by the TMA-DPH fluorescence increase accompanying the exocytosis phenomenon, as controlled by conventional titrations of the released histamine. TMA-DPH bound to the outer side of the plasma membrane of resting cells and additively to the inner side of granules connected by pores to the exterior of stimulated mast cells.

Animals↗
PubMed1985

Plasma membrane fluidity studies by fluorescence polarization in rat mast cells stimulated by compound 48/80.

Plasma membrane fluidity measurements were performed on purified living mast cells using a novel non-permeant fluorescence polarization probe TMA-DPH, upon stimulation by compound 48/80. The fluorescence anisotropy increased rapidly after treatment by 48/80 in a dose-dependent way. The effect was found to be specific for mast cells; it was inhibited by the histamine release antagonist FR 7534 in a correlative manner. The role of calcium was examined. The results brought evidence for a plasma membrane fluidity decrease induced by 48/80; a biphasic mechanism was inferred for the histamine release process.

Animals↗
PubMed1985

Calcium dependent modulation of histamine release from mast cells by sodium and potassium.

The inhibition of sodium-potassium ATPase by ouabain or potassium-deprivation led to a potentiation of histamine release induced by antigen or compound 48/80 from rat mast cells. The fullest potentiation required 30 min preincubation of cells with ouabain or without potassium before adding the triggering agent. The potentiation was observed provided that the calcium concentration was less than 0.5 mM. The effect of sodium-potassium ATPase blockade was reversed slowly by washing out ouabain or by adding potassium. Metabolic inhibition with deoxyglucose and dinitrophenol-blocked histamine release observed under all conditions described. Histamine release from rat mast cells was also elicited when the cells were incubated in sodium-deficient media where sodium was replaced by sucrose. Potassium-deprivation potentiated this secretion process previously shown to be dependent upon metabolic energy and sensitive to millimolar calcium concentrations.

Animals↗
PubMed1985

Kinetics of the inhibitory effect of flavonoids on histamine secretion from mast cells.

The effect of cromoglycate and of natural flavonoids on histamine release from peritoneal rat mast cells induced by compound 48/80 and ionophore A23187 was studied according to preincubation time of mast cells with drugs and to incubation time of cells with the triggering agent. Preincubation of cells with cromoglycate, dihydroquercetin and amentoflavone, a biflavonoid, decreased the potency of drugs to inhibit the ionophore-induced release; the optimal inhibitions were observed when drugs were added simultaneously with the ionophore A23187. In contrast, a short preincubation (2 min) of cells with quercetin or luteolin decreased their inhibitory effect on the ionophore-induced release, whereas a longer preincubation increased the inhibition. When compound 48/80 was used to trigger histamine secretion, the inhibitory potencies of all the compounds used were decreased according to preincubation time. Dihydroquercetin (taxifolin), previously considered as inactive, showed an interesting cromoglycate-like behaviour.

Animals↗
PubMed1985

Potential anti-anaphylactic activity of clenbuterol, a beta-agonist with calcium antagonist properties.

Clenbuterol 10(-8) to 10(-6) M inhibited antigen-induced histamine release from passively sensitized human lung tissue. This inhibition was not antagonized by propranolol, whereas the inhibitions observed with isoprenaline and fenoterol were reduced by propranolol. Clenbuterol also inhibited compound 48/80-induced histamine release and immunological histamine secretion from actively sensitized peritoneal rat mast cells. High concentrations of clenbuterol were required (10(-5) to 10(-3) M) and propranolol did not antagonize these inhibitions of histamine release. Isoprenaline and salbutamol did not modify the secretion from rat mast cells. The potential anti-anaphylactic activity of clenbuterol, might be partly related to its calcium antagonist property.

Adrenergic beta-Agonists↗
PubMed1985

[Cellular histamine liberation and mediators of anaphylaxis].

A study of the release of histamine from basophils and mast cells is clearly important to understand the mechanisms of activation of these cells and the anti-allergic mechanisms of the drugs in use. Important information has been gained through the study of highly purified rodent mast cells as well as human mast cells and basophils of low purity, in many fields: morphology, triggering mechanisms, degranulation and mediator release. Recent findings obtained with purified human mast cells and basophils could better identify the specific potential mediators of these two cells. Many biochemical events have been associated with anaphylactic mediator release: recent evidence suggested that an elevation of intracellular calcium level was an essential event in the processes by which mediators are released.

Anaphylaxis↗
PubMed1985

Transmembrane sodium and potassium gradients modulate histamine secretion induced by ionophore A23187.

Histamine secretion was induced from rat peritoneal mast cells by calcium ionophore A23187 in the presence of various extracellular calcium concentrations. Transmembrane sodium and potassium gradients were altered by cold pretreatment of mast cells or through the inhibition of sodium-potassium ATPase by the use of ouabain or potassium-deprivation. Such pretreatments led to a parallel shift to the left of the extracellular calcium concentration-histamine secretion curve, i.e. to an apparent decrease of extracellular calcium requirement for the ionophore-induced histamine release. These effects were fully reversed by warming mast cells, by washing out ouabain or by adding potassium. Metabolic inhibition of mast cells prevented the ionophore-induced secretion in all the experimental conditions described. Secretion observed in the absence of added calcium was inhibited by short term treatment of cells with 5 X 10(-6) M EGTA or EDTA provided magnesium was absent from the assay medium. Data show that ionophore A23187 was able to induce secretion in the presence of micromolar concentrations of extracellular calcium, when the efficiency of the ionophore was not decreased by extracellular magnesium and when transmembrane sodium and potassium gradients were altered.

Animals↗
PubMed1985

[Not Available].

Explore the source record for details and available documents.

Canada↗
PubMed1985

Physiological approach of beta receptor coupling to adenylate cyclase in rat airways: ontogenical modification and functional antagonism.

The relaxant effects of isoproterenol, forskolin and sodium nitroprusside were studied on tracheal pieces and lung parenchymal strips of Sprague-Dawley and Wistar rats according to age and functional antagonism with carbachol applied previously to induce the contraction. The beta receptor-related maximal relaxant effect of isoproterenol decreased from 4 to 11 weeks in Sprague-Dawley rat airways contracted with 10(-6) M carbachol. This maximal relaxant effect did not change with age in the Wistar strain. When lower carbachol concentrations were applied to Wistar trachea, the maximal relaxant effect of isoproterenol raised with a large decrease of the EC50 values. In the Sprague-Dawley strain, a similar diminution of carbachol concentration also allowed to increase the maximal amplitude of relaxation, but a smaller decrease of EC50 was observed as referred to the Wistar strain. These results suggest that the decrease with age of the maximal relaxation of Sprague-Dawley airways by isoproterenol might be linked to impaired functional antagonism between beta adrenergic and muscarinic stimulation in this rat strain. This hypothesis was strengthened by the observation of the effects of forskolin, an activator of adenylate cyclase, and sodium nitroprusside, a cyclic GMP-related relaxant drug, that did not show any modified effect in function of age in both rat strains. A modified regulation of adenylate cyclase complex with ontogenesis and with rat strain is suggested.

Adenylyl Cyclases↗
PubMed1984

Sodium-potassium ATPase inhibition potentiates compound 48/80-induced histamine secretion from mast cells.

The effect of ouabain on the histamine secretion induced by compound 48/80 has been studied using rat peritoneal mast cells. Ouabain did not modify histamine release in the presence of millimolar concentrations of extracellular calcium. However, when mast cells were previously washed with a calcium-free buffer, ouabain strongly potentiated histamine release elicited by compound 48/80. The full potentiation of mast cell secretion by ouabain required 30 min preincubation before adding compound 48/80. It was inhibited by lanthanum and EGTA. Potassium deprivation mimicked the effect of ouabain. A 30 min preincubation time without potassium was also required. Potassium concentrations below 2.7 mM increased the effect of ouabain whereas higher potassium concentrations reversed this effect. The potentiation of compound 48/80-induced histamine release by ouabain or potassium deprivation was not immediately reversed by washing away ouabain or by adding potassium, respectively. The data confirm that sodium-potassium ATPase is involved, through a calcium-dependent process, in the regulation of histamine release from mast cells.

Animals↗
PubMed1984

[Family life cycle in Quebec: comparative views, seventeenth to twentieth centuries].

A comparison of the family life cycle in Quebec at the end of the seventeenth century and in the middle of the twentieth century is presented. "For both periods, calculations of comparative indices were carried out in the absence of mortality and divorce. This allows the emphasizing of the outstanding features of the family life cycle....In particular, the considerable reduction in the duration of the extensive phase [is noted; this] is linked to the significant drop in fertility, and the emerging of a long phase of stabilization during which the parents are responsible for all their children. Finally, an examination of the proportion of undissolved families at each stage clearly shows the dramatic impact of mortality on family life in the past." (summary in ENG, SPA)

Americas↗
PubMed1983

Lanthanides are transported by ionophore A23187 and mimic calcium in the histamine secretion process.

Ionophore A23187 induced histamine release from peritoneal rat mast cells in the presence of lanthanum or terbium as it did in the presence of calcium. Low concentrations of lanthanides (10(-5) to 2 X 10(-4) M) were more efficient than similar concentrations of calcium. The effect of low concentrations of calcium and lanthanides were additive. Increasing the concentration of lanthanides above 10(-3) M decreased histamine release. This decrease was partly reversed by calcium. Calmodulin inhibitors, phenothiazines, R24571 and mepacrine, inhibited the histamine release induced by either calcium or lanthanides. Zn2+, a calmodulin inhibitor transported by A23187, inhibited more potently the calcium-dependent histamine release. Lanthanides decrease histamine release induced by 48/80 in the absence of added calcium. These data show that ionophore A23187 can transport lanthanides across the plasma membrane of mast cells, allowing the trivalent cations to substitute for calcium in the activation of calmodulin or calmoduline-like proteins.

Animals↗