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D J Chiarandini

Publications and source records attributed to D J Chiarandini.

28 records · Page 2Linked to original sources
PubMed1973

Effects of manganese on the electrical and mechanical properties of frog skeletal muscle fibres.

1. The effects of Mn on the electrical and mechanical properties of frog muscle fibres have been studied.2. In normal saline 10 or 20 mM-Mn hyperpolarized the fibres and had no effect on the membrane resistance. In isotonic K(2)SO(4) saline, Mn increased the membrane resistance indicating that this agent reduced the conductance to K.3. The action potential is prolonged by Mn while the overshoot amplitude is unaffected. The threshold of the action potential is shifted to more positive values of membrane potential.4. The isometric twitch is reduced by 45% in 10 mM-Mn; this effect is observed within 8 sec of the application.5. Mn (10 mM) reduced K contractures induced by 40 or 75 mM-K (constant [K].[Cl] product) and shifted to the right in a parallel manner the curve tension vs. log K concentration. The calculated mechanical threshold for K contractures was shifted from -48 to -33 mV.6. Caffeine contractures (3-4 mM) and supramaximal K contractures (190 mM-K) were unaffected by 10 mM indicating that contractile proteins and the ability of the sarcoplasmic reticulum to release Ca are not impaired.7. It is concluded that Mn is mainly affecting the excitation-contraction coupling by altering the mechanical threshold. Since Mn reduces the permeability to Ca in several excitable membranes, it is suggested that the mechanical threshold depends on the entry of Ca to the muscle.

Action Potentials↗
PubMed1970

Effects of caffeine on crayfish muscle fibers. I. Activation of contraction and induction of Ca spike electrogenesis.

Contractions are evoked in single muscle fibers of crayfish by intracellular as well as extracellular applications of caffeine. Responses to external applications in concentrations above 2 mM could be induced indefinitely. With concentrations above 5 mM the caffeine-induced responses were highly repeatable. Tensions were transient even when the caffeine remained in the bath. There was no change in resting potential, but during the contraction the effective resistance decreased about 10%. A number of factors (change in pH, Ca, K, and Cl) modified the responses. The time course of the tension was greatly prolonged when the transverse tubular system (TTS) was s swollen and was again shortened when the TTS was caused to shrink. An increased permeability to Ca induced by caffeine was evidenced by the transformation of the normally graded electrical responses to Ca spikes, which are insensitive to tetrodotoxin. The overshoot is a function of both external Ca and caffeine. A 10-fold change in Ca changed the overshoot by 19 mv in the presence of 10 mM caffeine and by 29 mv in 80 mM caffeine. The role of the increased permeability to Ca for caffeine-induced contractions will be analyzed in the accompanying paper.

Animals↗
PubMed1970

Effects of caffeine on crayfish muscle fibers. II. Refractoriness and factors influencing recovery (repriming) of contractile responses.

When caffeine evokes a contraction, and only then, crayfish muscle fibers become refractory to a second challenge with caffeine for up to 20 min in the standard saline (5 mM K(o)). However, the fibers still respond with contraction to an increase in K(o), though with diminished tension. Addition of Mn slows recovery, but the latter is greatly accelerated during exposure of the fiber to high K(o), or after a brief challenge with high K(o). Neither the depolarization induced by the K, nor the repolarization after its removal accounts for the acceleration, which occurs only if the challenge with K had itself activated the contractile system; acceleration is blocked when contractile responses to K are blocked by reducing the Ca in the bath or by adding Mn. Recovery is accelerated by redistribution of intracellular Cl and by trains of intracellularly applied depolarizing pulses, but not by hyperpolarization. The findings indicate that two sources of Ca can be mobilized to activate the contractile system. Caffeine mobilizes principally the Ca store of the SR. Depolarizations that are induced by high K(o), by transient efflux of Cl, or by intracellularly applied currents mobilize another source of Ca which is strongly dependent upon the entry of Ca from the bathing medium. The sequestering mechanism of the SR apparently can utilize this second source of Ca to replenish its own store so as to accelerate recovery of responsiveness to a new challenge with caffeine.

Animals↗
PubMed1967

Ionic mechanism of cholinergic inhibition in molluscan neurons.

Acetylcholine, the inhibitory transmitter to the so-called H-neurons of molluscs, produces its effect by increasing the permeability of the subsynaptic membrane to chloride ions. The change in permeability gives rise to a net influx of this anion, which hyperpolarizes the neuron. The presence of an outward pump of chloride ions is postulated to account for the required electrochemical gradient. The participation of potassium ions in this inhibitory phenomenon was not detected.

Acetylcholine↗
PubMed1967

Ionic mechanisms of cholinergic excitation in molluscan neurons.

Acetylcholine appears to be an excitatory transmitter at synapses on two different types of molluscan nerve cells: the so-called D- and CILDA neurons. The action of this substance is different in the two cases. In D-neurons, this compound increases the permeability of the subsynaptic or somatic membrane to chloride ions, and through a net efflux of this anion, depolarizes the cell. In CILDA neurons, on the other hand, acetylcholine depolarzies the cell by increasing its permeability to sodium ions.

Acetylcholine↗
PubMed1967

Two different ionic mechanisms generating the spike "positive" afterpotential in molluscan neurons.

The ionic bases of the "positive" afterpotential (ap) have been examined in the so-called DInhi neurons of the central nervous system of Cryptomphallus aspersa. In these cells E(K) has been determined and its value compared with the equilibrium, potential of the ap (E(ap)). It has been found that in half of the studied cells the E(K) value is very close to E(ap) whereas in another half, the difference (E(K) - E(ap)) is large and amounts to circa -10 mv. The effects of changes in the concentration gradients of K(+), Cl(-), and Na(+) were assayed in both groups of cells. When the [K(i)/[K](o) ratio is reduced in both groups of neurons, the ap amplitude and the E(ap) diminished. In cells displaying a large (E(K) - E(ap)), Cl-free Ringer's solution diminished the ap amplitude and E(ap), but produced no effect in the neurons with a reduced (E(K) - E(ap)). A similar effect was observed if [Cl], was increased by intracellular injection of NaCl. Changes in both [Na](o) and [Na](i) were ineffective. It is concluded that K(+) is the only ion involved in the origin of the ap in the groups of cells with a low value for (E(K) - E(ap)). On the contrary, the ap of the neurons presenting large (E(K) - E(ap)) is produced by a simultaneous increase in the fluxes of both K(+) and Cl(-).

Action Potentials↗