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Biomedical subjects

H GRUNDFEST

Publications and source records attributed to H GRUNDFEST.

At least 73 records · Page 4Linked to original sources
PubMed1954

Bioelectric effects of ions microinjected into the giant axon of Loligo.

1. A technique is described for recording the bioelectric activity of the squid giant axon during and following alteration of the internal axonal composition with respect to ions or other substances. 2. Experimental evidence indicates that the technique as described is capable of measuring changes in local bioelectric activity with an accuracy of 10 to 15 per cent or higher. 3. Alterations of the internal K(+) or Cl(-) concentrations do not cause the change in resting potential expected on the basis of a Donnan mechanism. 4. The general effect of microinjection of K(+) Rb(+), Na(+), Li(+), Ba(++), Ca(++), Mg(++), or Sr(++) is to cause decrease in spike amplitude, followed by propagation block. 5. The resting potential decreases when the amplitude of the spike becomes low and block is incipient. 6. The decrease in resting potential and spike amplitude may be confined to the immediate vicinity of the injection. 7. At block, the resting potential decreases up to 50 per cent, but injection of small quantities of divalent cations may cause much larger localized depolarization. 8. The blocking effectiveness of K(+), Na(+), and Ca(++) expressed as reciprocals of the relative amounts needed to cause block is approximately 1:5:100. Rb(+) has the same low effectiveness as does K(+). Li(+) resembles Na(+). Ba(++) and Mg(++) are approximately as effective as Ca(++). 9. Microinjection of Na(+) may cause marked prolongation of the spike at the injection site as well as decrease in its amplitude. 10. The anions used (Cl(-), HCO(3) (-), NO(3) (-), SO(4) (-), aspartate, and glutamate) do not seem to exert specific effects. 11. A tentative explanation is offered for the insensitivity of the resting potential to changes in the axonal ionic composition. 12. New data are presented on the range of variation, in a large sample, of the magnitude of the resting potential and spike amplitude.

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↗
PubMed1953

Mechanisms of bioelectric activity in electric tissue. I. The response to indirect and direct stimulation of electroplaques of Electrophorus electricus.

1. A preparation is described consisting of one or several layers of innervated cells of the electric organ of Electrophorus electricus. 2. Each plaque is multiply innervated and only at its caudal face. The nerve fibers may derive from two or more different nerve trunks. 3. During activity the innervated face becomes negative relative to the non-innervated. 4. The first electrical response of the cell to an increasing neural volley is graded and has the character of a prepotential. At a critical size of the prepotential the cell discharges with an all-or-nothing spike. 5. Both responses have durations of about 2 msec. 6. A neural volley which does not cause the spike discharge facilitates the discharge of the cell by a second subsequent volley in the same nerve (temporal facilitation). 7. The period of facilitation lasts ca. 900 msec. During the first 100 msec., the facilitation is large enough to cause a spike. In the later portion only the prepotential is facilitated. No electrical concomitant has been detected. 8. Neural volleys reaching the plaque from different trunks interact at the cell to produce a period of facilitation lasting only about 2 msec. This interaction is interpreted as spatial summation. 9. In a population of cells, simultaneous stimulation of 2 nerves causes a smaller discharge than the sum of the two isolated responses (occlusion). 10. Cells denervated for 7 weeks or more can be excited directly, but only by a current flow outward through the caudal face. 11. Weak direct stimulation causes a prepotential in the denervated plaque. On increasing the stimulus the prepotential increases to a critical size when a spike develops. The duration of both responses is about 2 msec. 12. The absolutely refractory period of the denervated cell is about 1.5 msec. and relative refractoriness lasts about 15 msec. 13. Direct stimulation causes slight facilitation lasting as long as 200 msec. 14. Repetitive stimulation of the nerve at low frequencies (2 to 3 per second) causes rapid "fatigue" of transmission. The denervated plaque, however, responds for several minutes to repetitive direct stimulation at high frequencies (25 per second).

Animals↗