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R Eckert

Publications and source records attributed to R Eckert.

At least 109 records · Page 6Linked to original sources
PubMed1982

Histamine-receptor bearing lymphocytes. II. The use of flow cytofluorometric analysis of histamine-receptors on mouse lymphocytes of different organs.

The histamine binding capacity of cells in various lymphoid organs has been determined by flow cytofluorometric (FCF) analysis of histamine receptors. Using fluoresceinated bovine serum albumin conjugated to histamine (HIS-BSA-FITC) as a staining reagent two distinct lymphocyte subpopulations of differing fluorescence intensity have been identified in each organ investigated. The thymus has a low number of histamine-receptor bearing cells, while bone marrow, lymph nodes and spleen reveal increasing binding capacities to the histamine conjugate. It is suggested that there exists a different susceptibility of distinct lymphocyte subpopulations for histamine, thereby enabling its controlled immunoregulatory activity.

Animals↗
PubMed1981

Calcium-mediated inactivation of the calcium conductance in caesium-loaded giant neurones of Aplysia californica.

1. The intracellular potassium in giant neurones of Aplysia californica was replaced with caesium by a method utilizing the ionophore nystatin. Because caesium ions have low permeability through potassium channels outward currents during voltage-clamp depolarization were strongly curtailed after the caesium loading procedure and the subsequent wash-out of the ionophore. 2. The calcium current elicited by a test voltage-clamp depolarization (pulse 2) was depressed following the entry of calcium elicited by a prior depolarization (pulse 1). 3. The percentage depression of the test current was a linear function of the pulse 1 current-time integral, and thus appears to be related linearly to the amount of calcium carried into the cell during pulse 1. This linear relation was maintained when calcium entry was varied by changes in external calcium concentration, by altered pulse 1 amplitude and altered pulse 1 duration. Depression was substantially reduced by injection of EGTA, and by substitution of barium for extracellular calcium. 4. The calcium current was unaffected by prior hyperpolarization of the membrane or by prior depolarizations to about ECa. Depression of the current was not altered by addition of extracellular 50 mM-TEA or by a strong hyperpolarization between the conditioning and test pulses. 5. The rate relaxation of the inward current during a given depolarization depended on the rate of entry and accumulation of free calcium. Relaxation under a given command potential became slower when calcium was partially replaced with magnesium so as to produce a smaller calcium current, or when accumulation of intracellular free calcium was retarded by injected EGTA or by barium substitution for extracellular calcium. 6 Evidence is considered that accumulation of calcium ions at the cytoplasmic surface of the membrane leads to inactivation through an action upon the calcium conductance. Reduced driving force and intracellular surface-charge neutralization do not adequately account for the observed depression of the calcium current resulting from intracellular accumulation of calcium ions.

Animals↗
PubMed1980

Calcium-mediated inactivation of calcium current in Paramecium.

1. The Ca current seen in response to depolarization was investigated in Paramecium caudatum under voltage clamp. Inactivation of the current was measured with the double pulse method; a fixed test pulse of an amplitude sufficient to evoke maximal inward current was preceded by a conditioning pulse of variable amplitude (0-120 mV).2. The amplitude of the current recorded during the test pulse was related to the potential of the conditioning pulse. Reduction of test pulse current was taken as an index of Ca current inactivation. The current recorded during a test pulse showed a progressive decrease to a minimum as the potential of the conditioning pulse approached +10 to +30 mV. Further increase in conditioning pulse amplitude was accompanied by a progressive restoration of the test pulse current. Conditioning pulses near the calcium equilibrium potential had only a slight inactivating effect on the test pulse current.3. Injection of a mixture of Cs and TEA which blocked late outward current had essentially no effect on the inward current or its inactivation.4. Elevation of external Ca from 0.5 to 5 mM was accompanied by increased inactivation of the test pulse current. The enhanced inactivation of the test pulse current was approximately proportional to the increase in current recorded during the conditioning pulse.5. Following injection of the Ca chelating agent, EGTA, the inactivation of the test pulse current was diminished; in addition, the transient inward current relaxed slightly more slowly, and the transient was followed by a steady net inward current.6. The time course of recovery from inactivation in the double pulse experiment approximated a single exponential having a time constant of 80-110 msec. Injection of EGTA shortened the time constant by as much as 50%.7. It is concluded that interference with the entry of Ca or enhanced removal of intracellular free Ca(2+) interferes with the process of Ca current inactivation, while enhanced entry of Ca promotes the process of inactivation. While the mechanism of inactivation is unknown, arguments are presented that the accumulation of intracellular Ca influences the Ca channel conductance.

Calcium↗
PubMed1980

Androgen-dependent sexual dimorphism of the immune system.

An androgen-dependent sexual dimorphism of the immune system was demonstrated in mice. The ration of T/B lymphocytes in the spleen was found to be significantly higher in adult females than in adult males. Furthermore, neonatal androgen administration in females gave rise to a permanent significant decrease of the T/B ratio, while neonatal castration in males resulted in a permanent increase of this ratio.

Animals↗
PubMed1978

Calcium entry leads to inactivation of calcium channel in Paramecium.

Under depolarizing voltage clamp of Paramecium an inward calcium current developed and subsequently relaxed within 10 milliseconds. The relaxation was substantially slowed when most of the extracellular calcium was replaced by either strontium or barium. Evidence is presented that the relaxation is not accounted for by a drop in electromotive force acting on calcium, or by activation of a delayed potassium current. Relaxation of the current must, therefore, result from an inactivation of the calcium channel. This inactivation persisted after a pulse, as manifested by a reduced calcium current during subsequent depolarization. Inactivation was retarded by procedures that reduce net entry of calcium, and was independent of membrane potential. The calcium channel undergoes inactivation as a consequence of calcium entry during depolarization. In this respect, inactivation of the calcium channel departs qualitatively from the behavior described in the Hodgkin-Huxley model of the sodium channel.

Animals↗
PubMed1978

Potassium activation associated with intraneuronal free calcium.

Relations between calcium entry and activation of a calcium-dependent outward current during depolarization were examined under voltage clamp in dorid giant neurons injected with the calcium-sensitive photoprotein aequorin. Activation kinetics and amplitude of the slow calcium-dependent component were both found to be related to the rate and extent of free calcium accumulation and to the electromotive force acting on potassium ions, independent of the calcium activation kinetics. This indicates that the activation of the calcium-dependent outward current is more closely related to the transient intracellular accumulation of free calcium ions than to the movement of calcium through the plasma membrane during depolarization.

Animals↗
PubMed1978

Calcium-dependent repolarization in Paramecium.

1. Intracellular injection, recording and current-passing methods were used to investigate the role of intracellular Ca in the modulation of electrical behaviour in the ciliate Paramecium caudatum.2. Injection of EGTA converted graded regenerative responses ascribed to Ca inward current to all-or-none action potentials. The EGTA injection also caused a discontinuity in the steady state I-V relations to outward current, but had little effect on hyperpolarizing current-voltage responses.3. The overshoot of the all-or-none spike produced by the EGTA-injected cell followed an approximate 29 mV increase for a tenfold increase in external Ca concentration and was independent of changes in external K and Na concentrations.4. The EGTA-induced all-or-none action potential tended to produce plateaus that could last up to 20 sec. During the plateau the membrane slowly repolarized to a critical potential, upon which repolarization occurred precipitously.5. Injection of 10(-6)M-free Ca(2+) as a Ca-EGTA buffer hyperpolarized the membrane and decreased the potential shifts to inward current pulses. These responses are consistent with an increase in K conductance.6. During EGTA plateaus reversed beating of the cilia indicated a rise in intracellular Ca, and thus an inability of the EGTA to complex the Ca as rapidly as it entered the cilia. Reversal of the motile apparatus thus appears to be activated at lower concentrations of intracellular Ca than are required to activate the inferred Ca-dependent K system.7. In uninjected cells removal of the cilia, which results in a loss of the voltage-activated Ca channels (Dunlap, 1977), or addition of extracellular Ba both tended to linearize the steady state I-V relations.8. Injections of Cs and TEA tended to linearize the steady state I-V relations, but did not result in either a conversion to an all-or-none spike or a discontinuity in the depolarizing steady-state I-V relations.9. It is concluded that in Paramecium a Ca-activated K conductance short-circuits the inward current of the regenerative Ca response, preventing all-or-none behaviour. The occurrence of plateau spikes following EGTA injection indicates that the Ca conductance inactivates very slowly in face of a maintained depolarization. Such slow Ca-inactivation is consistent with the slow relaxation of Ca-dependent ciliary reversal that occurs during maintained depolarization.10. The possibility is discussed that injection of EGTA may also enhance the Ca conductance.

Action Potentials↗
PubMed1978

An electrophysiological study of the regulation of ciliary beating frequency in Paramecium.

1. The role of the surface membrane in the control of ciliary beat frequency in Paramecium was examined by intracellular electrophysiological techniques and pressure injection of Ca2+ and EGTA. Experiments were done on wild type P. caudatum and on both the wild type and a pawn mutant of P. tetraurelia. 2. The increased frequency of beating that accompanies reversal of power stroke orientation in response to depolarization in the wild type fails to occur during depolarization in the mutant pawn, which also fails to exhibit ciliary reversal upon depolarization. 3. Injection of moderate amounts of EGTA blocked the frequency increase without interfering with reversal of the beat in response to depolarization of the wild type. Larger injection of EGTA also prevented reversed beating. 4. The beat frequency in the normal (forward-swimming) direction increased during hyperpolarization in pawn. The hyperpolarizing frequency-voltage relations were quantitatively similar to those of the wild type. 5. Injection of EGTA to a final concentration of 10 mM into wild type cells neither modified the resting frequency nor blocked the frequency increase which normally accompanies hyperpolarization. 6. Transient ciliary reversal in both pawn and wild type produced by injection of Ca2+ could be terminated by the passage of inward current. The power stroke returned to the normal forward-swimming direction and the ciliary beating frequency increased. Upon termination of the inward current the cilia of Ca2+-injected cells again beat in reverse for many seconds. 7. The results support previous reports that increased frequency of beating and ciliary reversal seen in response to depolarization both require the entry of Ca2+ through the surface membrane. On the other hand, the results indicate that frequency increase with hyperpolarization is independent of an altered rate of Ca2+ entry. 8. Increased frequency during hyperpolarization appears to be related more closely to electrotonic membrane current than to membrane potential. It is proposed that inward current might activate high frequency beating by altering the ionic environment of the axoneme within the restricted volume of the cilium by electrophoretic means.

Animals↗
PubMed1978

Studies on column fractionation of immune cells. VII. Electrophoretic mobility and functional behavior of mouse spleen cells after fractionation on a weakly basic ion exchanger.

After passing normal mouse spleen cells through columns of a weakly basic ion-exchanger, the percentage of cells with B cell-typical electrophoretic mobility (EPM) is 90% after fractionation at pH 8.0 and 10--20% at pH 5.0. However, the characterization of fractionated cells with regard to theta-antigen as well as graft-versus-host reaction shows that separation of T- and B-lymphocytes had not occurred. After incubation of the separated cells for 2 h at 37 degrees C the EPM returned to that of unseparated cells. It appears that the net charge of T- and B-lymphocytes is changeable depending on pH, temperature and separation material.

Animals↗
PubMed1977

Calcium-dependent depression of a late outward current in snail neurons.

Neuron cell bodies of Helix pomatia were voltage-clamped with a 300-millisecond depolarizing test pulse (pulse II) delivered I second after a depolarizing conditioning pulse (pulse I). The outward current, measured 200 milliseconds after the onset of pulse. II, exhibited a strong depression that was dependent on the presence of pulse. I. The maximum depression of the pulse II outward current occurred when pulse I voltages lay in the range over which calcium influx is inferred to be greatest; depression of the pulse II current subsided as pulse I potentials approached the putative calcium equilibrium potential. In the presence of extracellular [ethylenebis(oxyethylenenitrilo)]tetraacetic acid (EGTA) or D600, the intensity of the pulse II current became largely independent of pulse I, approaching the values of maximal depression seen in normal Ringer solution. On the other hand, lowering the intracellular pH with extracellular carbon dioxide-carbonate buffer had no measurable effect on the outward currents. Other experiments showed that it is primarily the calcium-dependent, outward-current hump of the N-shaped late current-voltage curve that is depressed by presentation of the conditioning pulse. It was concluded that distinct from an early potassium-activating role, calcium entering during a depolarization leads, during a subsequent depolarization, to a depression of the calcium-activated potassium system that persists for many seconds.

Action Potentials↗
PubMed1977

Voltage-dependent facilitation of Ca2+ entry in voltage-clamped, aequorin-injected molluscan neurons.

Voltage-clamp experiments were performed on giant neurons of the nudibranch Anisodoris nobilis injected with the Ca-sensitive photoprotein, aequorin. Depolarization beyond -10 to +5 m V produced an aequorin signal, the amplitude of which depended on the extracellular Ca2+ concentration, the amplitude of the depolarization, and its duration. In paired pulse experiments, the amplitude of the aequorin signal produced in response to the second of two identical depolarizing pulses was larger than that produced during the first, resulting from an increased entry of Ca2+ during the second pulse. The increment in Ca conductance inferred from the augmented signal during the second pulse was independent of Ca2+ influx during the first pulse but, instead, was related to the amplitude and duration of the first pulse.

Aequorin↗
PubMed1977

Lymphokines of T and B cells. I. Demonstration that T and B cells of tumor antigensensitised mice produce different lymphokines changing surface charge of target cells.

Lymphocytes from MC sarcoma-bearing mice were exposed to a soluble tumor antigen. The lymphokine-containing supernatant thus obtained was fractionated on Sephadex G-75. Fractions were tested for their activity to reduce the surface charge of indicator macrophages by cell electrophoresis technique. When unseparated spleen or lymph node cells were used the charge-reducing activity of the supernatant was found in three regions according to molecular weights of about 100,000, 60,000 - 35,000 and 13,000 Daltons. The appearance of activity was found to be time-dependent. As indicated by tests with separated lymphocytes both B and T cells appear to release charge-reducing activity.

Animals↗