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At least 811 records · Page 45Linked to original sources
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↗
PubMed1984

A mutation that alters properties of the calcium channel in Paramecium tetraurelia.

The membrane properties of a new mutant of Paramecium tetraurelia, dancer, were compared under voltage clamp with those of the wild type. The Ca2+ current was isolated and examined using CsCl-filled electrodes and tetraethylammonium in the bath solution to block K+ channels. The amplitude of the Ca2+ transient was not altered by the mutation. However, the Ca2+ current in the mutant inactivated more slowly and less extensively: hence a larger sustained Ca2+ current remained in the mutant. A change in the time course of the deactivation of the Ba2+ current was observed in the mutant. This mutational change is not likely to be the consequence of the Ca2+-channel inactivation because it is seen in the Ba2+ solution where there is little inactivation of the current. Other measured properties of the Ca2+ channel, the voltage-dependent K+ current, and the resting properties of the membrane were normal in the mutant. The Ca2+-activated K+ current and the Ca2+-activated Na+ current were larger in the mutant than in the wild type, consistent with a greater elevation of free intracellular Ca2+ during depolarization in the mutant. It is likely that the mutation causes an alteration in the Ca2+-channel structure or in its immediate environment and thereby affects the inactivation and deactivation processes of the Ca2+ channel. As would be expected from the greater Ca2+ current, the mutant tends to generate all-or-none Ca action potentials as opposed to the graded action potentials in the wild type.

Action Potentials↗
PubMed1985

Slow inactivation of the calcium current of Paramecium is dependent on voltage and not internal calcium.

The isolated Ca2+ current from Paramecium caudatum was examined under voltage clamp with long conditioning depolarizations lasting for up to 5 min. The isolated transient Ca2+ current inactivates with tens of milliseconds due to Ca2+ -dependent Ca2+ -channel inactivation (Brehm & Eckert, 1978). When this fast inactivation was blocked by internally delivered EGTA, a much slower inactivation of the Ca2+ current was discovered. This slow inactivation had time constants of tens of seconds, depending on voltage. The development of this slow inactivation was further examined by following the Ca2+ transient after 1 s interruptions of the long depolarization. This development is voltage dependent; the rate of inactivation is higher with a larger depolarization. After a long depolarization, the Ca2+ current returns in two clearly separable steps. A portion of the current returns rapidly along an exponential time course with time constants of tens to hundreds of milliseconds. The remainder of the current returns slowly with time constants of tens of seconds. A longer conditioning depolarization generates a larger portion that recovers slowly. Internally delivered EGTA, sufficient to prevent most of the fast inactivation, did not change the time course or the extent of either the onset or the removal of the slow inactivation. The compound W-7, which inhibits the Ca2+ current itself, does not block the onset of this slow inactivation during depolarization. We conclude that the slow inactivation of the Ca2+ channel is a mechanistically different phenomenon from the fast Ca2+ -dependent Ca2+ -channel inactivation. The possible physiological and behavioural roles of this slow inactivation are discussed.

Action Potentials↗
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↗
PubMed1959

Mutation in the protozoan Paramecium multimicronucleatum as a result of x-irradiation.

Mutations have been produced in the protozoan Paramecium multimicronucleatum by repeatedly exposing clonal cultures of the animals to large dosages of x-irradiation. The descendants of x-rayed survivors showed the following changes, which persisted in culture: destruction and loss of all micronuclei, decrease in vitality and reproductive rate, increase in x-radiation sensitivity, monstrosity, and reduced body size.

Animals↗
PubMed1992

Behavioral hypothermia and survival of hypoxic protozoans Paramecium caudatum.

Hypoxia has been shown to elicit behavioral hypothermia in a number of different metazoan species, all with nervous systems. The protozoan, Paramecium caudatum, has no nervous system and was not expected to display behavioral hypothermia. However, this species was also found to select a lower temperature in a thermal gradient under hypoxic conditions. This response proved to be beneficial as survival of hypoxic paramecia was greatly increased at lower temperatures. This unicellular species may provide a useful model to investigate the cellular and molecular basis of adaptive thermoregulatory behavior.

Animals↗
PubMed1967

Photoreactivation in vivo of pyrimidine dimers in paramecium DNA.

Cells of Paramecium aurelia labeled with tritiated thymidine were irradiated with ultraviolet light and then were either exposed to photoreactivating light or kept in the dark as controls. In the controls, the level of thymine-containing pyrimidine dimers did not change, but in cells exposed to photoreactivating light such dimers were destroyed. This is the first demonstration in a eukaryote of in vivo photoreactivation of thymine-containing pyrimidine dimers.

Animals↗
PubMed1969

Ionic mechanisms controlling behavioral responses of paramecium to mechanical stimulation.

A mechanical stimulus applied to the anterior part of Paramecium causes a transient increase in membrane permeability to calcium. This permits a calcium current to flow into the cell, causing the membrane potential to approach the equilibrium level for calcium. The transient depolarization which results elicits a reversal in the direction of ciliary beat. When the organisms are free-swimming this is seen as the reversed locomotion of Jennings' "avoiding reaction." In contrast, a mechanical stimulus applied to the posterior part results in increased permeability to potassium ions, and hence an outward potassium current. The hyperpolarization which results causes an increase in the frequency of ciliary beat in the normal direction. In free-swimming specimens this is seen as an increase in the velocity of forward locomotion.

Animals↗
PubMed1972

Reactivated triton-extracted models o paramecium: modification of ciliary movement by calcium ions.

Triton-extracted models of Paramecium were reactivated to swim in solutions of adenosine triphosphate and magnesium ions. The cilia beat in the normal direction (toward the rear) when the calcium ion concentration was less than 10-(6)M, and they beat in the "reversed" direction (toward the front) when calcium ion concentration was raised above 10-(6)M. These results support the proposal that ciliary reversal, hence backward swimming, of live paramecia is mediated by an increased cytoplasmic calcium concentration around the ciliary system by calcium-dependent membrane responses to external stimuli.

Adenosine Triphosphate↗
PubMed1973

Calcium-induced ciliary reversal in the extracted models of "Pawn", a behavioral mutant of Paramecium.

"Pawn," a genic mutant of Paramecium aurelia, cannot swim backward as the wild type can upon proper stimulation. In contrast, after membrane disruption by Triton X-100, the adenosine triphosphate-magnesium reactivated models of Pawns swim backward in the presence of calcium as wild-type models do. Thus, the mutant phenotype is due to an impairment in the membrane and not in the calcium-sensitive motile system.

Adenosine Triphosphate↗
PubMed1973

Temperature-sensitive pawns: conditional behavioral mutants of Paramecium aurelia.

"Pawns" are mutants of Paramecium aurelia in which the process of calcium activation during membrane excitation is genetically impaired, with a corresponding loss of avoiding reactions. Mutants are selected that behave normally when grown at 23 degrees C but as pawns at 35 degrees C. The normal excitation can now be disrupted and restored in the same strain at will.

Animals↗
PubMed1990

A magnesium current in Paramecium.

Recent reappraisals of the role of ionized magnesium in cell function suggest that many cells maintain intracellular free Mg2+ at low concentrations (0.1 to 0.7 mM) and that external agents can influence cell function via changes in intracellular Mg2+ concentration. Depolarization and hyperpolarization of voltage-clamped Paramecium elicited a Mg2(+)-specific current, IMg. Both Co2+ and Mn2+ were able to substitute for Mg2+ as charge carriers, but the resultant currents were reduced compared with Mg2+ currents. Intracellular free Mg2+ concentrations were estimated from the reversal potential of IMg to be about 0.39 mM. The IMg was inhibited when external Ca2+ was removed or a Ca2+ chelator was injected, suggesting that its activation was Ca2(+)-dependent.

Animals↗
PubMed1978

Paramecium fusion rosettes: possible function as Ca2+ gates.

The function of a specific intramembrane particle array, "the fusion rosette," an essential requirement for exocytosis of trichocysts in Paramecium, was probed with a temperature sensitive secretory mutant (nd9). The cells were grown at 27 degrees C, the nonpermissive, nonreleasing temperature at which fusion rosettes do not assemble. Exocytosis could be triggered, nonetheless, by addition of 40 micrometer ionophore A23187 and 15 mM Ca2+ but not Mg+. Rosette function is bypassed by this procedure, suggesting that during normal release, the rosette acts as a Ca2+ channel that allows development of a site-specific increase in Ca2+, which in turn induces fusion and release.

Biological Transport↗
PubMed1979

Membrane potential changes during chemokinesis in Paramecium.

Intracellular recordings show that (i) paramecia hyperpolarize slightly in attractants and depolarize in repellents that depend on the avoiding reaction (an abrupt change of swimming direction), and (ii) paramecia more strongly hyperpolarize in repellents and more strongly depolarize in attractants that depend on changes of swimming velocity. These membrane potential changes are in agreement with a hypothesis of membrane potential control of chemokinesis in Paramecium.

Animals↗
PubMed1984

Voltage-dependent calcium channels from Paramecium cilia incorporated into planar lipid bilayers.

Two different divalent cation-selective channels from Paramecium cilia were incorporated into planar lipid bilayers. Both channels were much more permeable to divalent than univalent cations, and one of them discriminated significantly among the divalent cations. The selectivity and voltage dependence of the latter channel are comparable to those of voltage-dependent calcium channels found in a variety of cells. A combined biochemical, biophysical, and genetic study of calcium channels is now possible.

Barium↗
PubMed1981

Mutagenicity of fly ash particles in Paramecium.

Paramecium, a protozoan that ingests nonnutritive particulate matter, was used to determine the mutagenicity of fly ash. Heat treatment inactivated mutagens that require metabolic conversion to their active form but did not destroy all mutagenicity. Extraction of particles with hydrochloric acid, but not dimethyl sulfoxide, removed detectable mutagenic activity.

Animals↗
PubMed1977

Saltatory motility of uninserted trichocysts and mitochondria in Paramecium tetraurelia.

In the subcortical regions of the ciliate Paramecium tetraurelia, mitochondria and uninserted trichocysts each display saltatory motility with individual characteristics, making them distinguishable from each other and from cellular cyclosis. The saltatory motion of trichocysts is implicated as the means of transporting new trichocysts from the cytoplasm to their ultimate locations in the cellular cortex. Saltatory motion may also be a factor in the intracellular distribution of mitochondria.

Animals↗