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E Rojas

Publications and source records attributed to E Rojas.

At least 217 records · Page 12Linked to original sources
PubMed1979

On the role of extracellular calcium in triggering contraction in muscle fibres from barnacle under membrane potential control.

1. Single giant barnacle muscle fibres from Megabalanus psittacus (Darwin) were used to establish the possible role of extracellular Ca2+ in triggering the contraction. 2. Peak tension p0 during twitches elicited by depolarizing voltage clamp pulses decreases after the removal of Ca2+ from the external saline. p0 becomes too small to measure after a few minutes, when the model-estimated level of total intracellular Ca has been reduced to 99.5% of its original value and the extracellular Ca in the clefts and/or tubules to about 10%. 3. In fibres where the outward currents were blocked by internal perfusion with Cs+, the curves of the integral of the inward current versus membrane potential and of peak tension versus membrane potential follow a similar pattern. 4. When Ca2+ in the external saline was replaced by Ba2+ or Sr2+, no twitches were generated although depolarizing voltage clamp pulses induced large inward currents comparable to those measured when Ca2+ was present. 5. It is concluded that an increase in Ca2+ in the fibre during the Ca2+ inward current is a necessary condition for the triggering of the development of tension. The data on Ba2+ inhibition is consistent with the hypothesis that there are two different intracellular sites of action for Ca2+.

Animals↗
PubMed1979

[Atherosclerosis].

Explore the source record for details and available documents.

Arteriosclerosis↗
PubMed1978

Asymmetrical displacement currents in the membrane of frog myelinated nerve: early time course and effects of membrane potential.

1. Asymmetrical displacement currents were studied in myelinated nerve fibres from Rana esculenta with a voltage clamp technique. 2. For brief pulses symmetrical with respect to a holding potential of--97mV, the asymmetry current flowing during pulses (on-response) exhibited a rising phase to a peak followed by an approximately exponential decline. After the pulses the rising phase in the off-response could not be resolved; the time constant varied about 2-fold with either size or duration of the pulse. 3. For longer pulses a second slower component could be detected both in on- and off-responses. 4. The rapidly declining on- and off-responses associated with brief pulses carried about the same charges Qon and Qoff. Increasing the duration of the pulse reduced Qoff. For all pulses tested Qoff approached about one fifth of Qmax. The reduction of Qoff was roughly characterised by time constants ranging between 1.5 and 0.5 ms for potentials between--25 and + 23 mV. Analysis of individual membrane currents confirmed that the capacity current after depolarizing pulses decreased with pulse length. 5. The effects of membrane potential on asymmetry current were studied by varying the level from which pulses were applied during 46.9ms prepulses in the range from--97 to--29mV. The fast and slow components of asymmetry current were affected differently. For potentials more positive than--90mV the fast on-response was reduced and reversed its sign at a potential 25mV more negative than the potential estimated from the steady-state charge distribution measured from--97mV.

Animals↗
PubMed1978

Cyclic changes in potential and resistance of the beta-cell membrane induced by glucose in islets of Langerhans from mouse.

1. The effects of KCl on the membrane potential were studied in cells from mouse islets of Langerhans identified as beta-cells by the characteristic pattern of electrical activity induced by 11.1 mM glucose. 2. In the absence of glucose, when the beta-cell membrane does not exhibit electrical activity, the dependence of the membrane potential upon external potassium [K+]o, could be described by the constant field equation using a PK/PNa ratio between 30 and 75. 3. In 11.1 mM glucose, when the beta-cell membrane potential fluctuates between a silent phase at about -50 mV and an active phase at about -40 mV giving rise to a train of spikes, the dependence of the membrane potential upon [K+]o could also be described with the constant field equation using a smaller PK/PNa of about 15, during the silent phase, and of about 8, during the active phase (foot of the spikes during the burst). 4. A bridge amplifier for measuring the changes in membrane potential during the application of pulses of current through the same micro-electrode was used to estimate the input resistance of a beta-cell. In 11.1 mM glucose, rough estimates of the membrane resistance during the silent phase averaged 1.2 X 10(8) omega. 5. The time course of the changes in input resistance of the cell when switching from 0 to 11.1 mM glucose showed a transient decrease from 0.9 X 10(8) to 0.7 X 10(8) omega followed by an increase to 1.2 X 10(8) omega. 6. The burst pattern was shown to result from the superposition of two potential changes: (a) 5--10 mV depolarization (lasting about 10 sec in 11.1 mM glucose), and (b) 10--50 mM spikes (lasting about 0.1 sec). Only the latter could be suppressed by hyperpolarizing current injection. 7. Application of pulses of current during the various phases of the electrical activity in 11.1 mM glucose enable us to compare the resistance during the silent and active phases. This was found to be oscillating between a high resistance value at about 1.2 X 10(8) omega before each burst and a low resistance value at 0.9 X 10(8) omega during the active phase at the foot of the spikes. In some cells the resistance during the silent phase remained fairly constant. In other cells it increased gradually from 1.1 X 10(8) to 1.3 X 10(8) omega measured just before each burst of spikes. 8. The observed increase in resistance induced by glucose together with the measured dependency of the membrane potential on [K+]o with and without glucose can be explained by postulating that in the presence of glucose the K+ permeability of the beta-cell membrane is reduced. 9. The oscillations between a high and a low resistance state in the presence of 11.1 mM glucose could be due to a sudden decrease in K+ permeability followed by a much larger increase in permeability to other ions, presumably Na+ and Ca2+.

Action Potentials↗
PubMed1976

Decreased rate of sodium conductance inactivation in the node of Ranvier induced by a polypeptide toxin from sea anemone.

The effects of two toxins extracted from the tentacles of Anemonia sulcata on ionic currents have been tested on the nodal membrane of myelinated nerve fibres from Rana esculenta. While external application of Toxin I at 100 muM leaves both specific ionic currents unmodified, Toxin II at 10 muM reacts with a receptor site associated with the sodium conductance inactivation gating. Since internal application by diffusion of Toxin II at a concentration of 700 muM leaves the ionic currents unchanged, the receptor site is most likely located on the external side of the nodal membrane. An equilibrium dissociation constant for the effects of Toxin II was estimated as 20 muM. The on-reaction is fast (rate constant for the on-reaction roughly equal to 3.103 M-1) suggesting a readily accesible receptor site for the toxin. The kinetics characteristics of the sodium currents recorded in the presence of Toxin II suggest that there are at least two steps in the reaction leading to Na+ -channels with the inactivation gate completely immobilized. The relatively fast reversibility of the intermediate stage of the reaction and the rather slow but, in the end, complete reversal of the toxin effects suggest that the toxin acts by modifying the energy profile for the transition "inactivation gate in the open configuration to inactivation gate in the closed configuration." Toxin II at higher concentrations (greater than 100 muM) also inhibits the potassium currents but these effects were not studied in any detail.

Animals↗
PubMed1976

[Inhibition of the sodium inactivation of the nodal membrane by anemonia sulcata toxin II].

A neurotoxin (ATX-II) extracted from the tentacles of Anemonia sulcata has been found to interact with the sodium channel of the nodal membrane in myelinated nerve fibres from Rana esculenta. If externally applied at low concentration (Kd = 20 muM), it reduces considerably the rate of inactivation of the sodium conductance without affecting the activation. At such concentrations, the potassium conductance is not affected. If internally applied ATX-II does not affect the membrane conductance.

Animals↗
PubMed1976

The temporal and steady-state relationships between activation of the sodium conductance and movement of the gating particles in the squid giant axon.

1. Comparisons were made between the kinetics and steady-state properties of the sodium conductance changes and of the sodium gating currents, in the squid giant axon perfused with caesium fluoride and maintained at a high membrane holding potential. The conductance measurements were made with reduced external sodium and as much electrical compensation as possible, in order to minimize errors caused by the series resistance. 2. After an initial delay of 10-150 musec whose size was a function of the holding potential and pulse amplitude, the conductance rise on depolarization followed cube law kinetics. 3. Values of the time constant taum, as defined by Hodgkin & Huxley (1952b), were determined for membrane potentials ranging between -140 and +70 mV. They lay on a nearly symmetrical bell-shaped curve with maximum (at 6-3 degrees C) of just under 500 musec at -36 mV. 4. Values of the gating current time constant tau(V) were determined over the same potential range, and found to lie on a very similar bell-shaped curve. A computed least-squares best fit gave the maximum as 460 musec, also falling at about -36 mV. 5. The midpoint of the minfinity curve lay at -34 mV, and its slope at this point was 0-0139 mV-1. Another series of measurements on intact axons gave a midpotential of -25 mV. In the perfused axons the state of the membrane was better described by the constant field equation than by gNa. Recalculation of minfinity from PNa shifted the curve about 15 mV in a positive direction.

Animals↗
PubMed1976

Destruction of the sodium conductance inactivation by a specific protease in perfused nerve fibres from Loligo.

Intracellular perfusion of giant axons from Loligo forbesi with a crude protein extract of Pronase dissolved in a KF solution suppresses the process of fast inactivation of the Na conductance (the h-process in the Hodgkin-Huxley terminology). 2. The results with protease inhibitors indicate that the most substrate specific endopeptidase present in pronase, alkaline proteinase b, destroys the h-process. 3. After destruction of the inactivation the conductance rise upon depolarization followed cube law kinetics. Values of the time constant taum before and after destruction of the h-process were very similar. 4. After destruction of the inactivation process the following properties were tested: cation selectivity, instantaneous conductance and internal receptor sites for tetrodotoxin (TTX) and tetraethylammonium (TEA). No detectable changes in selectivity or instantaneous conductance were observed. No internal receptors for TTX affecting the Na conductance were found but a TEA receptor is exposed by the protein hydrolysis. 5. TEA derivatives (triethylammonium, TEA-, with an aliphatic chain, Cn) induce a partial block of the steady-state sodium current and induce a time-dependent blockage of the conductance. 6. The first effect of TEA-Cn could be described in terms of a unimolecular reaction with the following equilibrium constants: 50, 2-5, 1-0, 0-4 and 0-025 mM for TEA-C2, TEA-C4, TEA-C5, TEA-C7 and TEA-C9 respectively. 7. From the dependence of the equilibrium dissociation constant on the length of the alkyl chain we estimated the free-energy change in 560 cal/mole of CH2. The gain in free energy per CH2 group transferred from aqueous medium to the interior of a non-polar medium is 1000 cal. 8. Although with the data at hand it is impossible to propose the amino-acid sequence of the site cleaved by alkaline proteinase b, we propose that an important functional component is arginine (or lysine).

Animals↗
PubMed1975

Effects of pH and ionic strength on the potassium system in the internally perfused giant barnacle muscle fibre.

Membrane potentials in single barnacle muscle fibres of Megabalanus psittacus, internally perfused with 200 mM K-acetate (KAc) solution of pH 7.5 were in the range --53 to --60 mV. These were followed as a function of pH of the external chloride saline. Decrease of pH of the Cl-saline from 8.5 to 3.5 hyperpolarized the membrane reversibly by about 8 mV. On further decrease of pH to 3.0, a transient hyperpolarization (from --60 to --65 mV) followed by a sudden and irreversible drop of potential to --40 mV was observed. Replacement of the external Cl-saline by acetate saline in the pH range 8.5 to 6.5 had no effect on the membrane potential. Further decrease of pH to 5.0 brought about an irreversible reduction of membrane potential. For fibres bathing in Cl- or Ac-saline at pH 7.5 when the internal pH was changed to 5.5, a transient hyperpolarization in Cl-saline and a sustained hyperpolarization in Ac-saline were observed. Further studies of membrane potential changing the concentration of external K, keeping the concentration of Cl or Ac constant, and changing the concentration of Cl or Ac, keeping the concentration of K constant, at different internal and external pHs showed that as the pH was reduced the membrane became more permeable to anions, Cl being more permeable than Ac. Experiments in which the membrane potential was controlled showed that when the internal pH of 200 mM KAc solution was reduced from 7.5 to 6.5 or raised to 8.5, the changes in outward K currents at various depolarizations were negligible. However, when the pH was reduced to 5.5 or 5.0, there was a progressive decrease in the outward K currents. The leakage currents in all these cases were relatively small. Use of high ionic strength solution of 580 mM KAc internally protected the K system in that when the pH was lowered the depression of the outward K current was smaller than that observed at a corresponding pH when the internal solution was 200 mM KAc. Use of low ionic strength solution of 50 mM KAc had the opposite effect. The results have been explained in terms of the ion exchange theory by postulating that the membrane has fixed amphoteric groups.

Acetates↗