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B Van Duijn

Publications and source records attributed to B Van Duijn.

9 recordsLinked to original sources
PubMed1992

Inositol trisphosphate-induced hyperpolarization in rat dorsal root ganglion neurons.

Inositol 1,4,5-trisphosphate (1,4,5-InsP3) was perfused into rat dorsal root ganglion (DRG) neurons by whole-cell patch-clamp electrodes, while measuring the membrane potential. This operation evoked a transient (2-3 min) membrane hyperpolarization of about -15 mV (from -42 mV) followed by a depolarization. The membrane hyperpolarization was abolished when 30 mM EGTA was perfused together with 1,4,5-InsP3 or when 0.2 mM quinine was added to the bath solution. The hyperpolarizing response was enhanced when a low-Ca2+ EGTA-free intracellular solution was used. Two InsP2 isomers induced a different response. Our results suggest that the hyperpolarization is due to 1,4,5-InsP3-induced Ca2+ release which may trigger Ca-sensitive K+ channels to open. Present results show that cultured DRG neurons are able to respond to 1,4,5-InsP3 perfusion in the whole-cell configuration.

Animals↗
PubMed1992

Independent control of locomotion and orientation during Dictyostelium discoideum chemotaxis.

Chemotaxis is cell movement in the direction of a chemical and is composed of two component: movement and directionality. The directionality of eukaryotic chemotaxis is probably derived from orientation: the detection of the spacial gradient of chemoattractant over the cell length. Chemotaxis was investigated in eukaryotic Dictyostelium discoideum cells that were permeabilized by high-voltage discharges. These permeable cells respond chemotactically to extracellular cAMP. However, locomotion is impaired if the Ca2+ concentration is clamped at submicromolar concentrations; interestingly, these non-motile cells still form pseudopodia and elongate in the direction of the cAMP gradient. These results imply that locomotion and orientation during Dictyostelium chemotaxis are independently regulated.

Animals↗
PubMed1991

Abscisic acid induces a cytosolic calcium decrease in barley aleurone protoplasts.

Cytosolic calcium concentrations (Cai) of barley aleurone protoplasts after stimulation with the plant hormone abscisic acid (ABA) were measured by using the calcium-sensitive fluorescent dye Indo-1. The measured basal Cai is about 200 nM. Stimulation with ABA induces a strong dose-dependent decrease in Cai to a minimal value of about 50 nM. This decrease occurs within 5 s. The Ca2+ antagonists La3+ and Cd2+ inhibit the ABA-induced Cai decrease in a dose-dependent manner, while the Ca2+ channel blockers verapamil and nifedipine give no inhibition. The induction of Cai decrease by ABA is consistent with activation of the plasma membrane Ca2(+)-ATPase by ABA. The possible role of this ABA-induced Cai decrease in ABA signal transduction and in counteracting the effects of gibberellic acid are discussed.

Abscisic Acid↗
PubMed1990

Chemoattractant-induced membrane hyperpolarization in Dictyostelium discoideum. A possible role for cyclic GMP.

Membrane potentials of the cellular slime mold Dictyostelium discoideum were monitored after chemotactic stimulation by measuring the distribution of the lipophilic cation tetraphenylphosphonium. Stimulation with the chemoattractant cAMP induces a transient membrane hyperpolarization which reaches its most negative value between 1-3 min after stimulation. This hyperpolarization is consistent with the opening of potassium channels. Measurements in streamer F mutant cells reveal that cGMP likely plays a role in the regulation of the cAMP-induced hyperpolarization.

Chemotaxis↗
PubMed1990

Normal chemotaxis in Dictyostelium discoideum cells with a depolarized plasma membrane potential.

We examined a possible role for the plasma membrane potential in signal transduction during cyclic AMP-induced chemotaxis in the cellular slime mold Dictyostelium discoideum. Chemotaxis, cyclic GMP and cyclic AMP responses in cells with a depolarized membrane potential were measured. Cells can be completely depolarized by two different methods: (1) by treatment with azide; this probably causes inhibition of the electrogenic proton pump, which was shown earlier to regulate plasma membrane potential in D. discoideum. (2) By electroporation, which causes the formation of large non-ion-selective pores in the plasma membrane. It was found that in depolarized cells the cyclic AMP-mediated cyclic AMP accumulation was inhibited. In contrast, chemotaxis to a cyclic AMP source was normal; the cyclic AMP-induced accumulation of cyclic GMP, which is known to mediate the chemotactic response, was also not affected. We conclude that membrane-potential-regulated processes, such as voltage-gated ion channels, do not play an essential role in chemotaxis in D. discoideum.

Cell Membrane↗
PubMed1989

A model study of the regulation of gastric acid secretion.

A computer simulation model is presented of the gastric phase regulation of gastric acid secretion in humans. The model is based on experimental data from the literature and includes terms representing gastric pH and gastric volume-dependent gastrin secretion, gastrin-dependent acid secretion, food storage in the stomach, and gastric emptying. We have explored the predictive value of the model in assessing the relative importance of gastric pH-dependent and gastric volume-dependent acid secretion mechanisms under various conditions. Similarly we have studied the role of gastric acid deregulation in achlorhydria, the Zollinger-Ellison syndrome, and duodenal ulcer, and the influence of the antacid drugs cimetidine and ranitidine under duodenal ulcer conditions. Model analysis of normal gastric acid regulation suggests that gastric volume-controlled acid secretion is of major importance during eating and predicts that pH-dependent gastrin secretion is of major importance in preventing excessively low pH levels between meals and during the night.

Achlorhydria↗
PubMed1988

Electrophysiological properties of Dictyostelium derived from membrane potential measurements with microelectrodes.

Electrical membrane properties of the cellular slime mold Dictyostelium discoideum were investigated with the use of intracellular microelectrodes. The rapid potential transients (1 msec) upon microelectrode penetration of normal cells had a negative-going peak-shaped time course. This indicates that penetration of a cell with a microelectrode causes a rapid depolarization, which can just be recorded by the microelectrode itself. Therefore, the initial (negative) peak potential transient value Ep (-19mV) should be used as an indicator of the resting membrane potential Em of D. discoideum before impalement, rather than the subsequent semistationary depolarized value En (-5 mV). Using enlarged cells such as giant mutant cells (Ep = -39 mV) and electrofused normal cells (Ep = -30 mV) improved the reliability of Ep as an indicator of Em. From the data we concluded that Em of D. discoideum cells bathed in (mM) 40 NaCl, 5 KCl and 1 CaCl2 is at least -50 mV. This potential was shown to be dependent on extracellular potassium. The average input resistance Ri of the impaled cells was 56 M omega for normal D. discoideum. However, our analysis indicates that the membrane resistance of these cells before impalement is greater than 1 G omega. Specific membrane capacitance was 1-3 pF/cm2. Long-term recording of the membrane potential showed the existence of a transient hyperpolarization following the rapid impalement transient. This hyperpolarization was associated with an increase in Ri of the impaled cell. It was followed by a depolarization, which was associated with a decrease in Ri. The depolarization time was dependent on the filling of the microelectrode. The present characterization of the electrical membrane properties of Dictyostelium cells is a first step in a membrane electrophysiological analysis of signal transduction in cellular slime molds.

Dictyostelium↗
PubMed1987

Ionic channels and membrane hyperpolarization in human macrophages.

Microelectrode impalement of human macrophages evokes a transient hyperpolarizing response (HR) of the membrane potential. This HR was found to be dependent on the extracellular concentration of K+ but not on that of Na+ or Cl-. It was not influenced by low temperature (12 degrees C) or by 0.2 mM ouabain, but was blocked by 0.2 mM quinine or 0.2 mM Mg2+-EGTA. These findings indicate that the HR in human macrophages is caused by the activation of a K+ (Ca2+) conductance. Two types of ionic channels were identified in intact cells by use of the patch-clamp technique in the cell-attached-patch configuration, low and high-conductance voltage-dependent K+ channels. The low-conductance channels had a mean conductance of 38 pS with Na+-saline and 32 pS with K+-saline in the pipette. The high-conductance channels had a conductance of 101 and 114 pS with Na+- and K+-saline in the pipette, respectively. Cell-attached patch measurements made during evocation of an HR by microelectrode penetration showed enhanced channel activity associated with the development of the HR. These channels were also high-conductance channels (171 pS with Na+- and 165 pS K+-saline in the pipette) and were voltage dependent. They were, however, active at less positive potentials than the high-conductance K+ channels seen prior to the microelectrode-evoked HR. It is concluded that the high-conductance voltage-dependent ionic channels active during the HR in human macrophages contribute to the development of the HR.

Cell Membrane↗