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Biomedical subjects

A M SHANES

Publications and source records attributed to A M SHANES.

At least 37 records · Page 2Linked to original sources
PubMed1955

Kinetics of ion movement in the squid giant axon.

The loss of Na(22), K(42), and Cl(36) from single giant axons of the squid, Loligo pealii, following exposure to an artificial sea water containing these radioisotopes, occurs in two stages, an initial rapid one followed by an exponential decline. The time constants of the latter stage for the 3 ion species are, respectively, 290, 200, and 175 minutes. The outflux of sodium is depressed while that of potassium is accelerated in the absence of oxygen; the emergence of potassium is slowed by cocaine, while that of sodium is unaffected. One cm. ends of the axons take up about twice as much radiosodium as the central segment; this difference in activity is largely preserved during exposure to inactive solution. Such marked differences are not observed with radiopotassium. From the experimental data estimates are given of the influxes and outfluxes of the individual ions. The kinetics of outflux suggests a cortical layer of measureable thickness which contains the ions in different proportions from those in the medium and which governs the rate of emergence of these ions from the axon as though it contained very few but large (relative to ion dimensions) pores.

Animals↗
PubMed1953

The effect of sodium and potassium ions on the impedance change accompanying the spike in the squid giant axon.

Decrease of the sodium concentration of the medium depresses both the spike and the associated impedance change in almost identical fashion. Elevation of the potassium level also depresses both phenomena, but affects the impedance change more than the spike; it slows the return to the initial impedance level. The effects on the threshold to brief square waves are also described. These results appear largely accounted for by the observations of Hodgkin and Huxley with the voltage clamp technique and by their recent hypothesis as to nature of the spike processes.

Animals↗
PubMed1953

Low level impedance changes following the spike in the squid giant axon before and after treatment with "veratrine" alkaloids.

The increase in conductance, which accompanies the spike in the presence of sea water, is followed by a decrease to below the resting level, here designated as the "initial after-impedance," which lasts 3 msec. and is 3 per cent as great as the increase. Treatment with cevadine usually obliterates the latter but leaves the former essentially unaltered. In addition, the alkaloid gives rise to periodic conductance increases followed by a prolonged, exponentially decaying elevated conductance (the "negativity after-impedance") which correspond closely to potential oscillations and to the negative after-potential. These are also only a few per cent of the major conductance change. Veratridine causes a conductance increase which lasts longer and which also conforms closely with earlier after-potential results. Preliminary calculations indicate that the negativity after-impedance and the negative after-potential may be due to the subsidence of an elevated chloride permeability. However, no satisfactory explanation is available for the initial after-impedance or for the temporal course of the conductance changes associated with oscillations in membrane potential.

Animals↗
PubMed1951

Potassium movement in relation to nerve activity.

The depolarization of crab nerve during repetitive stimulation is unaffected by the presence of glucose or by an increase in the calcium content of the medium. It is increased in both amplitude and rate by veratrine; in the presence of this alkaloid mixture the rate but not the magnitude of the depolarization is increased by an elevation in the calcium concentration. Repolarization following stimulation is unaltered by glucose and accelerated by a greater calcium concentration. Veratrine increases both the amplitude and the time constant of repolarization; its effect on the time constant is counteracted by an elevation of the calcium in the medium. Potassium released during stimulation and its reabsorption following activity have been observed by analyses of small volumes of sea water in contact with crab nerve. Under the conditions employed 3 x 10(-8) microM potassium is liberated per impulse per gm. wet weight of nerve. This loss is increased by low concentrations of veratrine, which also increase the amount reabsorbed during recovery. The depletion of potassium from the medium is appreciably less if the potassium previously released during activity has not been removed. Inexcitability resulting from anoxia can be washed away with oxygen-free solution-rapidly and completely in the case of the squid axon, slowly and incompletely in crab nerve. The potassium shifts are in the proper direction and of the correct order of magnitude to account for the negative and positive after-potentials in terms of potassium accumulation or depletion in the extracellular space.

Calcium↗
PubMed1950

Potassium retention in crab nerve.

Spectrophotometric determinations of the potassium content of small volumes of sea water brought into contact with crab nerves over half-hour intervals demonstrate (a) a continuous loss of potassium from the fibers while at rest in oxygen; (b) an appreciable increase in the leakage during anoxia; (c) a reabsorption of potassium during postanoxic recovery; and (d) a reduction in the amplitude of the anoxic and postanoxic changes in the presence of glucose.

Glucose↗
PubMed1950

Drug and ion effects in frog muscle.

Procaine, cocaine, pyribenzamine, antistine, and phosphate decrease the uptake of water by frog sartorii in a Ringer solution in which potassium has been substituted for sodium; all but the last two leave the swelling in hypotonic Ringer practically unaltered. They also decrease the depolarizing action of potassium. These effects are considered indicative of reduced membrane permeability to potassium.

Animals↗