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Biomedical subjects

E Rojas

Publications and source records attributed to E Rojas.

At least 199 records · Page 11Linked to original sources
PubMed1983

[Patterns of urinary aminoacid excretion in exceptional children and patients with mental disorders in Costa Rica].

The amino acid profile was studied in individual random samples of urine from 1147 normal schoolchildren and 1074 exceptional children: 628 with mental retardation, 332 with hearing and speech defects and 114 with visual defects as well as in 673 patients with mental disorders. Laboratory procedures included chemical tests and one-dimension paper- electro- and column-chromatography. Phenylketonuria was found in a mentally retarded girl and in one of her brothers; iminoglycinuria in a mentally retarded boy and heterozygote cystinuria in a man with manic-depressive psychosis. The percentage of high excretors of beta-aminoisobutyric acid (B-AIB) in the controls (4.88%) was similar to previous findings in the Caucasian race. The children with hearing and speech defects showed a number of high excretors of B-AIB significantly lower (X2 = 5.32; p less than 0.025) and the children with visual defects a number of hyperglycinurias significantly higher (X2 = 9.19; p less than 0.05). Previous non-consistent findings on the excess of high excretors of B-AIB in Down's syndrome were not confirmed in this study. These results suggest a relationship between transport defects in the plasma membrane and pathological disorders in some of the cases screened.

Alanine↗
PubMed1982

Sodium currents in the giant axon of the crab Carcinus maenas.

Measurements were made of the kinetics and steady-state properties of the sodium conductance changes in the giant axon of the crab Carcinus maenas. The conductance measurements were made in the presence of small concentrations of tetrodotoxin and as much electrical compensation as possible in order to minimize errors caused by the series resistance. After an initial delay of 10-150 microsec, the conductance increase during depolarizing voltage clamp pulses followed the Hodgkin-Huxley kinetics. Values of the time constant for the activation of the sodium conductance lay on a bell-shaped curve with a maximum under 180 microsec at -40 mV (at 18 degrees C). Values of the time constant for the inactivation of the sodium conductance were also fitted using a bell-shaped curve with a maximum under 7 msec at -70 mV. The effects of membrane potential on the fraction of Na channels available for activation studied using double pulse protocols suggest that hyperpolarizing potentials more negative than -100 mV lock a fraction of the Na channels in a closed conformation.

Animals↗
PubMed1982

Potassium currents in the giant axon of the crab Carcinus maenas.

Measurements were made of the kinetic and steady-state characteristics of the potassium conductance in the giant axon of the crab Carcinus maenas. These measurements were made in the presence of tetrodotoxin, using the feedback amplifier concept introduced by Dodge and Frankenhaeuser (J. Physiol, (London) 143:76-90). The conductance increase during depolarizing voltage-clamp pulses was analyzed assuming that two separate potassium channels exist in these axons. The first potassium channel exhibited activation and fast inactivation gating which could be fitted using the m3h, Hodgkin-Huxley formalism. The second potassium channel exhibited the standard n4 Hodgkin-Huxley kinetics. These two postulated channels are blocked by internal application of caesium, tetraethylammonium and sodium ions. External application of 4 amino-pyridine also blocks these channels.

4-Aminopyridine↗
PubMed1982

Potassium-induced insulin release and voltage noise measurements in single mouse islets of Langerhans.

Insulin release and membrane potential fluctuations in response to increased extracellular potassium [K+]o have been measured in single perifused islets of Langerhans from normal mice. An increase in [K+]o from 5 mM to 50 mM induced a transient insulin release with a peak at about 1 min. The peak value was [K+]o-dependent but the half-time t1/2 for the decline was constant at nearly 1 min. 2.5 mM cobalt completely inhibited the potassium-induced stimulation of insulin release. The insulin release elicited by 28 and 50 mM [K+]o was similar in terms of peak, total release and half-time from maximum release. Stepwise increase in [K+]o from 10 to 28 to 50 mM resulted in a normal response to 28 mM but no peak of release after the 28 to 50 mM increase. The results indicate good correlation between excess voltage noise, thought to reflect calcium channel activity, and insulin release evoked by changing extracellular potassium.

Animals↗
PubMed1982

Temperature dependence of the sodium channel gating kinetics in the node of Ranvier.

Temperature dependence of the Na+ channel gating kinetics was measured from the ionic and charge displacement currents in the node of Ranvier of Xenopus laevis, m3h kinetics was applied, assuming a delay, delta t, in the activation process. The rate constants for the m- and h-process showed Arrhenius temperature-dependence with Q10 of 2.34 and 2.9 respectively, while delta t exhibited non-Arrhenius temperature-dependence. Q10 for PNa, measured as 1.6, was smaller than for the rate constants and similar to that for a diffusion process. A negative shift and decrease in voltage sensitivity of the steady-state curves, h infinity and m infinity, occurred with decreasing temperature. The maximum time constant obtained from a single exponential fit to the displacement currents during the pulse for times greater than 90 microseconds exhibited Q10 of 2.01, which lies between that for PNa and that for tau m.

Animals↗
PubMed1982

Activation and inactivation characteristics of the sodium permeability in muscle fibres from Rana temporaria.

1. The steady-state and kinetic characteristics of the processes of activation and inactivation of the Na(+) permeability, P(Na), were measured in cut skeletal muscle fibres from Rana temporaria under voltage-clamp conditions.2. The specific resistance, r(ss), in series with the surface sarcolemma, was estimated as 6 Omega cm(2) by measuring the initial value of the membrane potential transient in response to current pulses under current-clamp conditions. To reduce the error in the potential across the sarcolemma introduced by r(ss), Na(+) currents were recorded using positive feed-back compensation, in the presence of tetrodotoxin (2.4-5 nm).3. P(Na)(t) was fitted with m(3)h kinetics assuming a voltage-dependent delay, deltat, to the start of the activation process.4. The P(Na)-V(p) curve exhibited saturation at potentials more positive than 30 mV. m(infinity), calculated as (P(Na), (infinity)/ P(Na))((1/3)) as a function of V(p), was a sigmoid curve with a mid point at -35 mV. The slope, dm(infinity)/dV(p), at this point was 0.032 mV(-1).5. Using a double-pulse protocol a non-exponential time course for the development of fast inactivation at small depolarizations was observed.6. The time constant for activation, tau(m), as a function of V(p), and tau(h) as a function of V(p), could be fitted with an approximately bell-shaped function, maximum of 430 mus at -43 mV and 925 mus at -78 mV respectively, at 15 degrees C.7. The mid-point potential of the h(infinity)-V(l) curve occurred at -58 mV, and h(infinity) approached 1 for V(1) values more negative than -103 mV.8. Using a double-pulse procedure the development of a slow inactivation of the Na(+) current was demonstrated. Its time course could be described in terms of a single exponential function, time constant equal to 0.58 s. The recovery from slow inactivation could be described by a similar exponential for recovery times smaller than 1 s.

Animals↗
PubMed1982

Fast charge movements in skeletal muscle fibres from Rana temporaria.

1. Fast charge movements were measured in cut skeletal muscle fibres from Rana temporaria.2. The initial time course of the current in response to a sudden displacement of the membrane potential from -110 to -60 mV was analysed in terms of an electrical equivalent circuit modified from Falk & Fatt (1964).3. The specific resistance in series with the sarcolemma was estimated as 7.4 Omega cm(2). The total capacity (surface sarcolemma plus tubular membrane) was estimated as 3.43 muF/cm(2).4. The asymmetry currents settling within 1 ms during depolarizing pulses of increasing size (on-response), from a holding potential around -120 mV, could be described in terms of a single exponential. The asymmetry currents after the pulses (off-response) exhibited at least two components.5. The integral of the on-response, Q(on), as a function of V(p), could be fitted using a function of the Boltzmann type. At the mid-point of the distribution curve, equal to -38 mV, the slope was 0.012 mV(-1). A saturating value of 28 pC was reached at 40 mV.6. The off-response to pulses not exceeding 3 ms exhibited two components. The first one had an exponential time course. The charge Q(off) associated with this fast component was always equal to Q(on).7. tau(on) (the relaxation time constant), as a function of membrane potential was asymmetrical, exhibiting a maximum value of 233 mus at about -38 mV.8. For V(p) values smaller than -20 mV the Q(on)-V(p) and tau(on)-V(p) curves could be analysed using the two-state transition model. From this analysis the average transition potential V' was estimated as -38 mV and the effective valence of the mobile charges as 1.36.9. Double-pulse protocols (duration of pre-pulses referred to as T in the range 0-3 s) showed that Q(on) and tau(on) decreased as T increased. Single transient analysis shows that the changes are confined to the transient for depolarizing pulses.10. This immobilization of the charges is reversible and follows a similar time course to the slow inactivation of the Na(+) conductance described in the preceding paper.11. A differential effect of the depolarizing pre-pulse on the ionic and asymmetry currents is seen in the decrease of tau(on) with increasing T while tau(m) remains constant.

Animals↗
PubMed1981

A method for the simultaneous measurement of insulin release and B cell membrane potential in single mouse islets of Langerhans.

A method has been developed for the simultaneous measurement of insulin release and electrical activity in single micro-dissected mouse islets of Langerhans. The effects of D-glucose have been studied in individual islets. Each islet was exposed to 0, 5.6, 11.1, 16.7, 22.2, 27.8, and 33.3 mmol/l glucose in a stepwise fashion. The minimum glucose concentration required to elicit spike activity is lower than that required to stimulate insulin release above basal levels and the maximum spike frequency occurs at a lower glucose concentration than does maximum insulin release. Following a reduction in glucose from 27,8 (or 33.3) to 5.6 mmol/l, membrane potentials returned to resting values within 2 min whereas insulin returned to basal values after 20 min. Increasing glucose from 5.6 to 27.8 mmol/l induced spike activity within 10 s; the insulin response was detected within 40 s. Thus, it is possible to use the single mouse islet for simultaneous measurements of insulin release and electrical activity.

Animals↗
PubMed1981

Voltage noise measurements across the pancreatic beta-cell membrane: calcium channel characteristics.

1. Membrane potential fluctuations were measured in cells from mouse Islets of Langerhans identified as beta-cells by the characteristic pattern of electrical activity induced by 11 mM-D-glucose. 2. The membrane potential was controlled by adjusting the external potassium concentration, [K+]o, keeping the sum [Na+]o plus [K+]o constant. In the absence of glucose, when [K+]o is raised, the resulting depolarization is accompanied by a significant increase in voltage noise. 3 The amplitude and time course of the voltage noise were measured under various experimental conditions. The variance of the fluctuating voltage decreased monotonically along the depolarization induced by sudden increase in [K+]o, suggesting a monotonic reduction in the number of elementary events. 4. The frequency characteristics of the excess noise could be analysed as the sum of 1/f and 1/f2 components. While the 1/f component remained unaffected by the external application of 20mM-tetraethylammonium (TEA) and either 2 mM-Mn2+ or 2 mM-Co2+, the 1/f2 component was suppressed by both Mn2+ and Co2+. 5. The corner frequency, fc, of the 1/f2 component depended on membrane potential, which was adjusted by adjusting the [K+]o jump. These results support the idea that fc in these experiments is a measure of the channel relaxation. 6. Measurements of the input resistance in the frequency range from 0 to 25 Hz were used to obtain a rough estimate of the size of the channel conductance as 5 x 10(-12) omega (-1).

Animals↗
PubMed1980

Diffusion models for the squid axon Schwann cell layer.

The Schwann cell, basement membrane, and connective tissue layers that surround the squid giant axon and constitute barriers to diffusion, were modeled in a number of ways to analyze various experimental results. The experiments considered are (a) the time-course of the potassium concentration in the space between the Schwann cell and the axon membrane (from now on referred to as the F-H space) after an initial loading, (b) the time-course of sodium concentration in the F-H space after a sudden change in the sodium concentration in the external fluid; (c) the time-course of the concentration of tetrodotoxin (TTX) or saxitoxin (STX) in the F-H space after a sudden change in external concentration, including (or not) the effects of specific binding of TTX or STX to sites on the axon membrane and nonsaturable binding to sites in the F-H space or in the spaces (clefts) between Schwann cells; (d) the effects of the F-H space, clefts, and diffusion into the clefts from the outside (from now on referred to as convergence into the clefts) on the measured series resistance.The analysis shows that (1) in no case is it necessary to include the effects of the convergence into the clefts from the outside; (2) in case a, the basement membrane, connective tissue layers, and the unstirred layer may be neglected, i.e., the clefts are rate limiting; (3) in case b the clefts may be neglected, i.e., the unstirred layer is rate limiting; (4) in most cases the clefts may be replaced by an equivalent thin diffusion barrier.

Animals↗
PubMed1980

Resting metabolism of inorganic phosphorus and changes during mechanical activation in perfused muscle fibres from Balanus.

The levels of inorganic phosphorus (Pi), arginine (and indirectly N-phosphoryl arginine) and adenosine triphosphate (ATP) were measured in intact and perfused muscle fibres from the barnacle Megabalanus psittacus, in resting conditions and during mechanical activity. A twitch caused the liberation of Pi to the intracellular perfusion solution and there was a corresponding decrease in the content of N-phosphoryl arginine of the muscle fibre. Mechanical activation did not induce a significant change in the level of ATP, but since the technique did not allow fast changes in ATP to be observed, the possibility that there was breakdown of ATP followed by a rapid resynthesis cannot be ruled out.

Adenosine Triphosphate↗
PubMed1980

The nature of the oscillatory behaviour in electrical activity from pancreatic beta-cell.

The typical burst pattern of electrical activity recorded from beta-cells of mouse islets in the presence of 11.1 mM glucose has been compared from 225 cells in terms of two parameters: relative duration of the active phase and periodicity of the oscillations between active and silent phases. The two parameters show different distributions, Gaussian and bimodal respectively. Burst periodicity was found to increase dramatically at external potassium concentrations below 2mM, while the relative duration of the active phase was little affected at concentrations as low as 0.5 mM. Increasing external calcium concentration significantly increased the amplitude of the bursts but greatly decreased the relative duration of the active phase. Quinine, in the absence of glucose, induced depolarization and electrical activity and stimulated insulin release from perifused mouse islets; spike frequency and insulin release followed a monophasic pattern. A model has been proposed for the beta-cell explaining the experimental results in terms of a feedback mechanism between calcium permeability activated by depolarization of the cell membrane and potassium permeability activated by an increase in the concentration of intracellular ionized calcium [Ca2+]i. The results are in agreement with the hypothesis that a [Ca2+]i-dependent potassium permeability, specifically blocked by quinine, controls membrane potential and insulin release.

Action Potentials↗
PubMed1979

Mouse pancreatic beta-cells: tetraethylammonium blockage of the potassium permeability increase induced by depolarization.

1. Membrane potentials and input resistance were measured in beta-cells from mouse pancreatic islets of Langerhans in the presence or absence of D-glucose. 2. Tetraethylammonium (TEA) (a specific blocker of the K permeability increase induced by shifts in membrane potential from negative to positive values) was externally applied and its effects on potentials and input resistance evaluated. 3. In the absence of glucose, addition of TEA up to 20 mM to the perifusion medium did not affect the resting potential and the input resistance, the selectivity ratio PK/PNa (calculated from the constant field equation) remaining unchanged at about 30. 4. The characteristic response of the beta-cell membrane potential, in the presence of glucose, is a fluctuation between a silent phase at about -50 mV and an active phase at about -40 mV giving rise to a train of spikes. TEA abolishes this pattern and very much reduces the graded response of spike frequency normally seen with different concentrations of glucose. 5. Addition of glucose in the presence of up to 20 mM-TEA induces an increase in membrane resistance of about 4.10(7) omega. 6. TEA lowers the glucose level required to trigger the electrical activity from about 5.6 to about 4.6 mM. 7. TEA blocks the repolarization phase of action potentials induced by the addition of glucose or by depolarizing intracellular current injection. 8. In the presence of 11.1 mM-glucose and 20 mM-TEA the action potentials frequently crossed the zero line, the membrane potential reaching up to 25 mV during the peak of the spikes.

Action Potentials↗
PubMed1979

Potassium permeability activated by intracellular calcium ion concentration in the pancreatic beta-cell.

1. Membrane potentials and input resistance were measured in beta-cells from mouse pancreatic islets of Langerhans in a study designed to assess the role of a K permeability specifically blocked by quinine or quinidine and activated by intracellular calcium ion concentration ([Ca2+])i-activated PK). 2. Addition of 100 microM-quinine to the perifusion medium resulted in a 10--30 mV depolarization of the membrane and an increase in the input resistance of ca. 4.10(7) omega. 3. In the absence of glucose, 100 microM-quinine induced electrical activity. 4. In the presence of glucose, 100 microM-quinine abolished the burst pattern of electrical activity and very much reduced the graded response of spike frequency normally seen with different concentrations of glucose. 5. Addition of mitochondrial inhibitors, KCN, NaN3, DNP, CCCP, FCCP, to the perifusion medium containing glucose rapidly hyperpolarized the beta-cell membrane, inducing a concomitant decrease in input resistance. 6. In the presence of glucose, these mitochondrial inhibitors reversibly blocked electrical activity; upon removal of the inhibitor, recovery of electrical activity followed a biphasic pattern. 7. The effects of mitochondrial inhibitors were partially reversed by 100 microM-quinine. 8. It is proposed that the membrane potential of the beta-cell in the absence of glucose is predominantly controlled by the [Ca2+]i-activated PK. It is further suggested that this permeability to K controls the level for glucose stimulation and leads to the generation of the burst pattern.

Action Potentials↗