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G de Bruin

Publications and source records attributed to G de Bruin.

9 recordsLinked to original sources
PubMed1984

Single potassium channel conductance in the frog node of Ranvier.

The single K+-channel conductance was calculated from the variance of the spontaneous potassium noise currents in voltage clamped frog node. Essential for this calculation is the mean potassium conductance during the noise measurement. So far this quantity has been underestimated, apparently due to K+-ion accumulation. With the proper values, the single K+-channel conductance is an increasing function of membrane voltage.

Animals↗
PubMed1983

Synchronization in chains of pacemaker cells by phase resetting action potential effects.

Interactions between pacemaker cells in a chain were calculated according to a "phase-reset" model. It is based on effects of action potentials in the cells on the cycle lengths of neighbouring cells. These effects were defined for each cell by a latency-phase curve (LPC), giving the latency time (L) until the onset of the next action potential in that cell, as a function of the phase (phi) at which a neighbour cell fired an action potential. Neighbour cells with simultaneous action potentials did not influence each others cycle length. We investigated how stable synchronization depends on the shape of the LPC's of the pacemaker cells and on chain length. Three types of interactive behaviour were distinguished. First, anti-phase synchrony, in which neighbouring cells fired with large phase differences with respect to the synchronized period Ps. Second, asynchrony, in which the periods of the cells did not become equal and constant. Third, in-phase synchrony, in which the phase differences between the neighbouring cells were zero or much smaller than the synchronized period Ps, depending on the differences between the intrinsic periods. Asynchrony and anti-phase synchrony may be seen as cardiophysiological arrhythmias, while in-phase synchrony represents the physiological type of synchrony in the heart. In-phase synchrony appeared to be strongly favoured by LPC's, which have a no-effect (refractory) part at early phases, a lengthened latency (or phase delay) part at intermediate phases and a shortened latency (or phase advance) part at late phases in the cycle. Such LPC-shapes are commonly found in preparations of cardiac pacemaker cells. When the pacemaker cells were identical, the synchronized period Ps during in-phase synchrony was equal to their intrinsic period P*i. For different intrinsic periods, Ps was equal to the intrinsic period of the fastest cell if the LPC's contained a sufficiently long initial no-effect period at early phases and a shortened latency part at late phases. When, on the other hand, such cell chains had a linear gradient in their intrinsic periods, "action potentials" started from the fast end and traveled along the chain. The propagation of an action potential wave slowed down as it reached the slower cells. When the gradient in the intrinsic periods was too steep, only the intrinsically fast end of the chain developed synchrony.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1982

Suppression of pacemaker activity by rapid repetitive phase delay.

Spontaneous activity of pacemaker cells of structures may be suppressed by rapid repetitive stimulation. Conditions are that the oscillator's phase reset curve, characterizing the phase resetting effect of single stimuli, has a phase delay part and that the interval between the stimuli falls within a range of values, determined by the form of the phase reset curve. Under these conditions, which appeared the same as those for stable underdrive pacing, the pacemaker becomes stably entrained to the stimuli without firing, i.e. it is kept within a certain part of its limit cycle because the pulses repeatedly delay the next coming action potential. This rapid stimulation suppression of pacemaker activity is demonstrated experimentally on a simple electronic pacemaker cell model for two types of phase reset curves, a biphasic one for depolarizing and a monophasic one for hyperpolarizing pulses. Computer simulations of coupled pacemaker cells, interacting by phase reset curves, illustrate how this type of pacemaker suppression may protect a population of pacemaker cells like the sinus node in the heart against arrhythmias.

Animals↗
PubMed1982

Conditioning prepulses and kinetics of potassium conductance in the frog node.

The kinetics of potassium conductance were analyzed in response to voltage-clamp steps with holding potential (-75 mV) as initial condition and after a positive prepulse towards +45 mV of 10-msec duration. As the potassium reversal potential EK altered during potassium current flow, a method to obtain the conductance independent of EK was used. Conductance kinetics at 15 degrees C were analyzed according to the Hodgkin-Huxley (HH) model. The time constant of potassium activation, with holding potential as initial condition, is a monotonous decreasing function of membrane potential. Its value of ca. 9 msec at -50 mV decreases to 1 msec at +30 mV. Changes in EK did not affect the voltage dependency of this time constant. The time constant of potassium deactivation, i.e. the off-response following a 10-msec prepulse towards +45 mV, shows a completely different voltage dependency. At a membrane potential of -90 mV it is approximately 2 msec and gradually increases for more positive voltages towards a maximum value of about 6 msec, that is reached between -5 and 0 mV. At still larger values of membrane voltage this time constant starts to fall again. It is concluded that a HH-model, as applied for a single population of potassium channels, has to be rejected. Computer simulations indicate that an extension to two populations of independent potassium channels, each with HH-kinetics, is also inconsistent with the observed results.

Animals↗
PubMed1982

Effect of purified phospholipases on glucose transport, insulin binding, and insulin action in isolated rat adipocytes.

The influence of alterations in phospholipid structure by phospholipase treatment on insulin action and glucose transport in rat adipocytes was studied. It appeared that phospholipase A2 from bee venom caused a breakdown of approximately 50% of phosphotidylcholine without lysis of the cells. Because of this treatment, insulin binding was increased, resulting in an increased sensitivity of glucose transport towards lower insulin concentrations. Moreover, an increased affinity of the transport system for 2-deoxyglucose was observed. Phospholipase C from Clostridium welchii caused complete lysis of adipocytes. Phospholipase A2 from Crotalus adamenteus was without effect.

Adipose Tissue↗
PubMed1981

Influence of environmental temperature on mitochondrial membranes.

Mitochondrial phospholipids from goldfish lateral line muscle were analysed with respect to polar and apolar groups. Groups of 20 goldfish, acclimated to 5, 20 and 30 degrees C, were used. Temperature-induced shifts of both polar and apolar groups of the mitochondrial phospholipids were observed. The fatty acid composition of mitochondrial phospholipids is characterized by a large amount of polyenoic acids, dominated by docosahexaenoic acid and by octadecadienoic acid. At the higher acclimation temperatures, a significant decrease in docosahexaenoic acid is found. However, the resultant effect of environmental temperature on the degree of unsaturation is small, in contrast to the marked effect on mean chain length. Pronounced changes in the molar ratio of phosphatidylcholine and phosphatidylethanolamine are seen; a decrease in mitochondrial phosphatidylcholine is observed at low acclimation temperature, which is compensated for by a nearly equal increase in phosphatidylethanolamine. The main phospholipids are, apparently, phosphatidylcholine, phosphatidylethanolamine and cardiolipin, comprising 90% of the total pool of 12 species. It is found that the anionic nature of the phospholipids is increased at low acclimation temperatures. We discuss this effect and its probable importance in the stabilization of the surface potential of the mitochondrial membranes.

Acclimatization↗