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D Landowne

Publications and source records attributed to D Landowne.

23 records · Page 2Linked to original sources
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↗
PubMed1971

Analysis of the potential-dependent changes in optical retardation in the squid giant axon.

1. An analysis has been made of the change in optical retradation of the membrane elicited by the application of voltage-clamp pulses in squid giant axons.2. The retardation response consists of three separate voltage-dependent components. For freshly mounted axons, defined as being in state 1, hyperpolarizing pulses give a rapid increase in the light intensity measured with crossed polarizers which has been termed the fast phase. This is followed by a rather slow return towards the base line termed the rebound. On treatment of the axon with certain agents that include tetrodotoxin, high calcium and terbium, the rebound disappears and the fast phase slows down, increases in size, and has a new slow component added to it. This transition from state 1 to a second state, 2, appears to be irreversible.3. In state 1, the time constant of the fast phase is 20-40 musec at 13 degrees C; it has a very large negative temperature coefficient (Q(10) = Ca.(1/8)). The size of the retardation change is independent of temperature and varies as the square of the applied voltage, but the voltage-retardation curve is symmetrical about a point well beyond zero membrane potential, at an internal potential of around + 70 mV. In state 2, the time constant is about five times larger, and varies much less markedly with temperature; the apex of the voltage-retardation curve is shifted to + 200 mV.4. The rebound has a time constant of the order of 20 msec at 13 degrees C. A 10 degrees rise in temperature more than halves the time constant and roughly doubles the amplitude of the rebound. The voltage dependence of the rebound differed from that of the fast phase.5. The slow component of state 2 has a time constant of about 2 msec which does not change noticeably between 10 and 25 degrees C. The size of this component seems to be linearly dependent on the applied voltage, rather than obeying a square law.6. A tenfold increase in external calcium concentration had no discernible effect on the fast and slow phases, but reversibly reduced the amplitude of the rebound nearly to half.7. In experiments on perfused axons, the retardation response was not measurably altered by any of the modifications made to the composition of the perfusing fluid.8. There was some indication of the possible existence of a small current- or conductance-dependent component of the retardation response.9. These phenomena seem likely to originate either from molecular relaxation processes analogous with the Kerr effect, or from changes in membrane thickness under the influence of the pressure exerted by the electric field. However, the specific molecules involved in the retardation response cannot yet be identified.

Animals↗
PubMed1970

The binding of tritiated ouabain to mammalian non-myelinated nerve fibres.

1. A study has been made of the binding of radioactively labelled ouabain by desheathed rabbit vagus nerves, which consist mainly of non-myelinated fibres. The corresponding inhibition of the electrogenic sodium pump was also measured.2. By varying the ouabain concentration and the external potassium concentration two kinds of binding sites could be distinguished: a first site specifically associated with pumping and whose ability to bind ouabain is dependent on the external presence of potassium; and a second site not associated with pumping and unaffected by external potassium.3. Just complete inhibition of the sodium pumping mechanism is associated with a specific binding of ouabain of about 4.3 p-mole/mg dry nerve.4. This gives an upper limit for the density of sodium pumping sites of about 750 per square micron.5. The turnover rate (i.e. (cation pumped)/(number of sites)) at 20 degrees C is about 22 sec(-1).

Animals↗