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R W Straub

Bio: R W Straub is an academic researcher. The author has contributed to research in topics: Vagus nerve. The author has an hindex of 1, co-authored 1 publications receiving 12 citations.
Topics: Vagus nerve

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TL;DR: The extra efflux with stimulation seems to result predominantly from an increase in intracellular inorganic phosphate resulting from increased break‐down of ATP after activity.
Abstract: 1 The movements of labelled phosphate were measured in garfish olfactory and in rabbit vagus nerves at rest and during activity 2 In garfish olfactory nerve kept in solutions with 120 mM-sodium and 02 mM-phosphate the fractional loss of 32P was 982 X 10(-4) min-1 Lowering the sodium concentration of the washing fluid decreased the efflux; lowering the phosphate produced a transient increase with subsequent return towards the efflux in 02 mM-phosphate 3 Stimulation at 050 sec produced an extra fractional loss of 12 X 10(-6) impulse-1 At 1/sec the effect was larger; at 5/sec it was about the same as at 05/sec 4 After stimulation the effect of activity disappeared exponentially with a time constant of 44 min 5 Lowering the sodium decreased the extra efflux with stimulation, whereas changing the phosphate concentration did not much affect the extra efflux 6 In rabbit vagus nerve kept in 154 mM-sodium and 02 M-phosphate the fractional loss of 32P was 491 X 10(-4) min-1 Lowering the sodium or the phosphate decreased the resting efflux 7 Stimulation of the vagus nerve at 15/sec produced an extra fractional loss of 087 X 10(-6) impulse-1 8 The extra efflux with stimulation seems to result predominantly from an increase in intracellular inorganic phosphate resulting from increased break-down of ATP after activity

12 citations


Cited by
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TL;DR: Topographic patterns of clinical deficit are reviewed and it is suggested that lesions distributed at random along the length of the entire fiber may result in dysfunction that exhibits distinct proximal-distal gradients.
Abstract: Pathophysiologic and clinicopathologic aspects of diabetic nerve disease are reviewed Abnormal modes of impulse conduction in diseased nerves include decreased conduction velocity, tempor

35 citations

Journal ArticleDOI
Jörgen Ekström1
TL;DR: The findings discussed in this paper indicate that the capacity to form the neurotransmitter acetylcholine, as judged by the activity of choline acetyltransferase, is influenced by the traffic of nerve impulses, as a long term effect.
Abstract: The findings discussed in this paper mainly derived from studies on salivary glands, serving as model organs, indicate that the capacity to form the neurotransmitter acetylcholine, as judged by the activity of choline acetyltransferase, is influenced by the traffic of nerve impulses, as a long term effect. In the glands, choline acetyltransferase seems to be exclusively localized to the cholinergic nerves. In the postganglionic parasympathetic nerves of the glands, the activity of choline acetyltransferase decreases when the flow of secretory impulses in these nerves is abolished or reduced either by isolating the nerves from the central nervous system, surgically or pharmacologically, or by diminishing the reflex activation of the glands from the mouth. The opposite occurs when the reflex activation of the salivary glands is enhanced, i.e. the activity of choline acetyltransferase increases. Observations on various other organs are quoted in support of the view that the traffic of nerve impulses is of importance for the activity of the enzyme. An increase, in choline acetyltransferase activity also occurs in some salivary glands after sympathetic denervation. This puzzling observation is discussed in relation to impulse traffic. Increased nerve impulse traffic and collateral sprouting seem to be responsible for the rapid restitution of choline acetyltransferase activity from a low level in an organ partially deprived of its cholinergic nerve supply.

31 citations

Journal ArticleDOI
TL;DR: It is concluded that although changes in metabolism of the nerve produce changes in the phosphate efflux expected on the basis of the concomitantChanges in the internal concentration of inorganic phosphate, the converse is not true; and increases and decreases in the rate constant of phosphorous efflux do not necessarily signal the corresponding metabolic changes.
Abstract: 1. A comparison has been made between the efflux of labelled phosphate from the non-myelinated fibres of the desheathed rabbit vagus nerve at 37 degrees C and the corresponding O2 consumption at rest and during activity, and during a variety of experimental interventions. 2. The resting rate constant of phosphate efflux was 2.61 X 10(-3) min-1: electrical stimulation (10 sec-1, 3 min) produced an extra fractional loss of 6.75 X 10(-6) impulse-1. 3. The corresponding resting O2 consumption was 0.484 m-mole x kg-1 impulse-1. 4. Ouabain (100 microM) produced a sustained depression (of about 40%) of the resting O2 consumption, accompanied by a transient fall (of about 14%) in the rate constant of phosphate efflux. 5. Na salicylate (10 mM) or Na arsenate (1 mM) produced a much larger increase in phosphate efflux than in resting O2 consumption. 6. Changing the external phosphate concentration (between 0.02 and 2 mM), addition of acetylcholine (1.7 mM), and addition of lanthanum (20 microM)--all of which are known to affect markedly the phosphate efflux in rabbit non-myelinated fibres--had little or no effect on the resting O2 consumption or, where tested, on the extra O2 consumption with electrical stimulation. 7. Changing the external Ca concentration (between 0.09 and 9 mM) had only minor effects on the O2 consumption (resting and stimulated) and on the rate constant of resting phosphate efflux. 8. It is concluded that although changes in metabolism of the nerve produce changes in the phosphate efflux expected on the basis of the concomitant changes in the internal concentration of inorganic phosphate, the converse is not true; and increases and decreases in the rate constant of phosphate efflux do not necessarily signal the corresponding metabolic changes.

23 citations

Journal ArticleDOI
TL;DR: The oxygen consumption and the movements of labelled phosphate were measured in garfish olfactory nerve at rest and during activity.
Abstract: 1. The oxygen consumption and the movements of labelled phosphate were measured in garfish olfactory nerve at rest and during activity. 2. In solutions with 2·5 mM-K and 0·2 mM-phosphate the resting oxygen consumption was 0·206 m-mole/kg.min; activity at 2 sec-1 produced an extra oxygen consumption of 2·46 μmole/kg.impulse. The extra oxygen consumption declined exponentially with a time constant of 2·62 min at 22-26 °C. 3. The phosphate efflux, measured simultaneously, had a resting efflux rate constant of 1·24 × 10-3 min-1; activity at 2 sec-1 produced an extra fractional loss of 9·38 × 10-6 impulse-1. The increase in phosphate efflux followed almost the same time course as the increase in oxygen consumption. 4. Increasing the frequency of stimulation from 2 sec-1 to 3 or 5 sec-1 decreased both the extra oxygen consumption and the extra fractional loss of phosphate. When the frequency was decreased to 0·5 or 1 sec-1 the extra oxygen consumption per impulse increased, while the extra phosphate liberation was lowered. 5. Changing the phosphate concentration did not much affect the extra oxygen consumption; on the other hand, lowering or increasing the phosphate from the standard 0.2 mM decreased both the resting and the stimulated phosphate efflux. 6. Lowering the K from the standard 2·5 mM did not affect the extra oxygen consumption, but increased both the resting and the extra loss of phosphate. At higher K concentrations the extra oxygen consumption and the extra fractional loss of phosphate decreased without much change in the resting phosphate efflux. 7. Application of 1-20 μM-strophanthidin produced a transient decrease in the resting phosphate efflux without much change in resting oxygen consumption. With 10 or 20 μM-strophanthidin the extra fractional loss of phosphate and the extra oxygen consumption were both lowered in approximately the same proportions. 8. The findings are consistent with the hypothesis that the increase in intracellular inorganic phosphate that results from increased break-down of ATP after activity, is the main cause for the increased phosphate efflux. A fraction of the increase in intracellular phosphate only appears to be liberated to the outside, the value of the fraction depending on the resting phosphate efflux before activity. 9. The initial increase in intracellular inorganic phosphate after an impulse, estimated from the oxygen consumption or the phosphate fluxes, appears to be about 12-19 μmole/kg nerve, remarkably close to the value known from chemical analysis.

21 citations