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D Landowne

Publications and source records attributed to D Landowne.

13 recordsLinked to original sources
PubMed1990

Chloramine-T alters the nerve membrane birefringence response.

The change in birefringence during depolarizing voltage-clamp pulses of internally perfused squid giant axons are biphasic. There is a rapid decrease in birefringence with a 220-microsec half time at 8 degrees C followed by a slow decrease over the next several milliseconds. After the pulse there is a rapid recovery which is smaller than the initial rapid decrease followed by a slow recovery phase. The rate of change of the slow phase during the pulse is more rapid for larger depolarizations. After the pulse the rate of change is more rapid for more negative potentials. 3.6 mM chloramine-T, applied externally until the sodium currents were prolonged and inactivation was removed, removed the slow phase of the birefringence response both during and after the pulse and made the fast 'off' response as large as the fast 'on' response. Two anesthetics reduced the birefringence response by about 20%. A rocking helix model is presented which relates the birefringence findings and earlier gating current experiments.

Animals↗
PubMed1987

D2O and the sodium pump in squid nerve membrane.

In 10 K artificial seawater (ASW), D2O replacement reduced the Na efflux of squid axons by about one third. In 0 K ASW, D2O replacement had little effect. D2O reduced the K+ sensitivity of the efflux but increased the affinity for K+. A 4 degrees decrease in temperature mimicked the effects of D2O. When axons were injected with arginine, to decrease the ATP/ADP ratio, they lost K+ sensitivity in normal ASW, as expected. Their efflux into 0 K ASW became D2O sensitive. The results are discussed in terms of conformational changes in the Na pump molecular complex.

Animals↗
PubMed1985

Molecular motion underlying activation and inactivation of sodium channels in squid giant axons.

Measurements of the changes in birefringence associated with changes in membrane potential were made with internally perfused squid giant axons in low sodium solutions at 0-8 degrees C. The time course of the birefringence changes share many properties of the 'gating' (polarization) currents previously studied in this nerve. Both can be demonstrated as an asymmetry in the response to voltage pulses symmetrical about the resting potential which is not present about a hyperpolarized holding potential. Both have a rapid relaxation, which precedes the sodium permeability change. Both exhibit an initial delay or rising phase. Both are reversibly blocked by perfusion with 30 mM or 300 nM tetrodotoxin. The birefringence response has a decrease in the amplitude of the rapid relaxation associated with the appearance of a slow relaxation. This is similar to the immobilization of fast gating charges which parallels sodium current inactivation. The amplitude of the birefringence and the gating current responses is consistent with a change in the alignment of several hundred peptide bonds per sodium channel.

Animals↗
PubMed1977

Sodium efflux from voltage clamped squid giant axons.

1. The efflux of radioactive sodium was measured from squid axons during simultaneous voltage clamp experiments such that it was possible to determine the efflux of sodium associated with a measured voltage clamp current. 2. The extra efflux of sodium associated with voltage clamp pulses increased linearly with the magnitude of the depolarization above 40 mV. A 100 mV pulse of sufficient duration to produce all of the sodium current increased the rate constant of efflux by about 10(-6). 3. Application of 100 nM tetrodotoxin eliminated the sodium current and the extra efflux of radioactive sodium. 4. Cooling the axon increased the extra efflux/voltage clamp pulse slightly with a Q10 of 1/1-1. On the same axons cooling increased the integral of the sodium current with a Q10 of 1/1-4. 5. Replacing external sodium with Tris, dextrose or Mg-mannitol reduced the extra efflux of sodium by about 50%. The inward sodium current was replaced with an outward current as expected. 6. Replacing external sodium with lithium also reduced the extra efflux by about 50% but the currents seen in lithium were slightly larger than those in sodium. 7. The effect of replacing external sodium was not voltage dependent. Cooling reduced the effect so that there was less reduction of efflux on switching to Tris ASW in the cold than in the warm. 8. The extra efflux of sodium into sodium-free ASW is approximately the same as the integral of the sodium current. Adding external sodium produces a deviation from the independence principle such that there is more exchange of sodium than predicted. Such a deviation from prediction was noted by Hodgkin & Huxley (1952c). 9. Using the equations of Hodgkin & Huxley (1952c) modified to include the deviation from independence reported in this paper and its temperature dependence, one can predict the temperature dependence of the sodium efflux associated with action potentials and obtain much better agreement than is possibly without these phenomena. 10. This deviation from independence in the sodium fluxes is the type expected from some kind of mixing and binding of sodium within the membrane phase.

Animals↗
PubMed1976

The temperature dependence of the movement of potassium and chloride ions associated with nerve impulses.

1. The influx and efflux of radioactive potassium and chloride across the membrane of the squid giant axon were measured in resting and in stimulated nerves. The measurements were made at room temperature and at 6-8 degrees C. 2. At room temperature all eight flux measurements were comparable to previously reported values. 3. When the axons were cooled the resting potassium influx decreased with a Q10 of 1-9 and the resting potassium efflux decreased with a Q10 of 1-2. 4. With cooling the resting chloride efflux decreased with a Q10 of 1-3 and the resting chloride influx decreased with a Q10 of 2-8. This latter value, together with anomalous flux ratios for resting chloride fluxes may indicate an active uptake of chloride ions into the axon. 5. Cooling increased the extra efflux of potassium associated with nerve impulses with a Q10 of 1/1-5 and increased the extra influx of potassium with a Q10 of 1/3-3. 6. No extra efflux of chloride was detected at either temperature. Cooling produced no statistically significant change in the extra chloride influx but there was considerable scatter in the data. 7. Fluxes were computed as a function of temperature for standard action potentials with a variety of temperature coefficients for the conductances and rate constants. No single curve could match either the influx or the efflux data.

Action Potentials↗
PubMed1975

A comparison of radioactive thallium and potassium fluxes in the giant axon of the squid.

1. The influx and the efflux of 204Tl and 42K were measured in intact squid giant axons. 2. The resting efflux of 204Tl was found to be about one half of 42K and to have a temperature coefficient (Q10) of 1-3 as compared to 1-1 for K. 3. The extra efflux of 204Tl associated with nerve impulses was 30% greater than 42K. 4. From either Cl or NO3 sea water, the resting influx of 204Tl was about three times that of 42K. Ouabain reduced the influx of either isotope by about two thirds without changing the Tl/K ratio of the fluxes. This indicates that the Na pump can transport Tl. 5. From NO3 sea water the extra influx of 204Tl assoicated with nerve impulses was about the same as 42K. From Cl sea water there was no detectable extra influx of 204Tl. 6. The flux ratio, ouabain-insensitive influx/efflux, was different for the two ions. The resting flux ratio for Tl was consistent with a passive non-interacting flux, whereas K movements were consistent with 'single file' passage through the membrane. 7. The extra flux associated with nerve impulses is different from the resting flux both in Tl/K selectivity and in the effect of anion in the sea water. There is also a much higher flux per unit time during the nerve impulse. These differences suggest differences in the mechanisms underlying ion permeability at rest and during nervous activity.

Action Potentials↗
PubMed1974

The temperature dependence of the movement of sodium ions associated with nerve impulses.

1. The movement of sodium ions across the membrane of the squid giant axon was measured by the use of radioactive tracers. Unidirectional fluxes were measured at rest and when the nerve was stimulated. The difference was considered the extra flux association with nerve impulses.2. The extra influx in intact axons at room temperature was 5.5 p-mole/cm(2). impulse. At 6 degrees C the extra influx was 6.5 p-mole/cm(2). impulse giving a Q(10) of 1/1.2.3. In perfused axons a Q(10) of 1/1.6 was obtained for the extra sodium influx in bracketed experiments on individual axons.4. The Q(10) of the extra sodium efflux associated with nerve impulses was found to be 1/1.2 in intact axons.5. Hodgkin & Huxley had predicted a much larger temperature dependence for the extra fluxes. If this difference between prediction and experiment does not result from some experimental error, then the class of models for the ion fluxes suggested by Hodgkin & Huxley may be inapplicable.

Animals↗
PubMed1971

Optical studies on the kinetics of the sodium pump in mammalian non-myelinated nerve fibres.

1. A study has been made of the changes in the fluorescence of desheathed rabbit cervical vagus nerves that occur during and after electrical stimulation of its non-myelinated fibres.2. Stimulation for 5 sec at 30 shocks/sec produces a maximal decrease, of about 1% of the resting fluorescence. Stimulation for less than 0.5 sec fails to produce responses visible above the inherent noise in the recording system.3. A pharmacological dissection (with ouabain, metabolic inhibitors, and calcium) has revealed four phases of fluorescence change:(a) under conditions where the sodium pump is functioning, there is a prolonged decrease in the fluorescence following electrical activity;(b) even in the absence of pumping the mere entry of sodium into the nerve causes an initial decrease in fluorescence;(c) the entry of calcium ions with electrical activity also causes an initial rapid decrease in fluorescence;(d) following these phases of decreased fluorescence there is a phase of increased fluorescence.4. These changes in fluorescence are related to changes in the NADH concentration in the nerve resulting from:(a) the splitting of ATP during sodium extrusion;(b) the initial binding of sodium to the sodium- and potassium-dependent ATPase, which is the sodium pump;(c) the stimulation of mitochondrial respiration by calcium that has entered during the spike; and(d) an increased glycogenolysis as a result of the calcium entry during activity.

Action Potentials↗
PubMed1971

On the control of glycogenolysis in mammalian nervous tissue by calcium.

1. A study has been made of the increase in fluorescence of the desheathed cervical vagus nerve that occurs after electrical stimulation (usually 5 sec at 30/sec) of its non-myelinated fibres.2. At room temperature this increase in fluorescence is normally masked by the decrease in fluorescence caused by mitochondrial oxidative phosphorylation. However, at higher temperatures (30-35 degrees C) the increasing fluorescence phase predominates and the net change on stimulation is an increase.3. At room temperature the increase in fluorescence is seen clearly only when ATP splitting has been prevented by ouabain, by bathing the nerve in lithium-Locke solution, or when oxidative phosphorylation has been prevented by metabolic inhibitors.4. The increasing fluorescence response is absent when calcium is removed from the external medium; it increases with increasing calcium concentration.5. It is argued that the increasing fluorescence response is due to an increase in glycogenolysis (leading to an increase in the reduced pyridine nucleotide concentration) brought about by the increased calcium entry during the action potential. This calcium presumably increases the activity of phosphorylates a or phosphofructokinase.6. Calcium entry also speeds mitochondrial oxidative phosphorylation.

Action Potentials↗