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Journal ArticleDOI

Effects of azide and chloretone on the sodium and potassium contents and the respiration of frog sciatic nerves

20 May 1958-The Journal of General Physiology (The Rockefeller University Press)-Vol. 41, Iss: 5, pp 959-988

TL;DR: With the exception of 15.0 mM chloretone the ionic shifts produced by these reagents may be due primarily to the depression of the respiration, although there are indications that azide acts, in addition, by another pathway.

AbstractAzide (0.2 to 5.0 mM) and chloretone (2.0 to 15.0 mM) reversibly inhibited 20 to 90 per cent of the resting respiration of frog sciatic nerves, and caused a loss of potassium and a gain of sodium in this tissue. The changes in ionic contents that developed after 5 or 10 hours were roughly correlated with the degree of respiratory depression, but the time courses of these changes were different with the two reagents. In azide these changes appeared to begin immediately, while in chloretone, at concentrations between 3.0 and 5.0 mM, the ionic shifts developed after a delay of several hours. Fifteen millimolar chloretone produced immediate changes in ionic contents several times greater than those produced by anoxia. The changes in ionic distribution produced in 5 hours by anoxia, 5.0 mM azide, or 5.0 mM chloretone were at least partially reversible; those produced by 15.0 mM chloretone were irreversible. With the exception of 15.0 mM chloretone the ionic shifts produced by these reagents may be due primarily to the depression of the respiration, although there are indications that azide acts, in addition, by another pathway. Concentrations of azide or chloretone that depressed the resting rate of oxygen consumption more than 50 per cent produced a slow conduction block, while 15.0 mM chloretone blocked conduction within 15 minutes.

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110 citations


Journal ArticleDOI
TL;DR: Motor nerve terminals in magnesium‐poisoned rat hemidiaphragm‐phrenic nerve preparations in vitro were stimulated with short depolarizing pulses of approximately threshold strength and the evoked antidromic responses recorded from the phrenics nerve, and the excitability of the terminals was depressed.
Abstract: 1. Motor nerve terminals in magnesium-poisoned rat hemidiaphragm-phrenic nerve preparations in vitro were stimulated with short depolarizing pulses of approximately threshold strength and the evoked antidromic responses recorded from the phrenic nerve. The percentage of these 1/sec or 0·5/sec stimuli to which there was no antidromic response was used as a quantitative measure of the terminal excitability. After standard tetanic stimulation (1000 impulses at 100/sec) the excitability of the terminals was depressed for an average duration of 60-70 sec, during most of which time no antidromic responses to stimuli of pretetanic intensity were recorded. There was no significant interaction between stimuli to the terminals at rates of 1 or 0·5/sec. 2. Potassium-free solutions at first increased, then decreased, the post-tetanic depression of excitability. Raising [K]o threefold (15 m M) abolished the post-tetanic depression and often converted it to an exaltation of excitability. 3. Polarizing currents were applied to the terminals with a second electrode. Depolarizing currents increased, while hyperpolarizing currents decreased, the post-tetanic depression of excitability. 4. In solutions with 70% of the normal NaCl content replaced by sucrose, the post-tetanic depression of excitability was reversibly prolonged. 5. In the presence of 7·7 × 10−6 M digoxin or 0·42 m M ouabain there was a small reversible reduction of post-tetanic excitability. 6. After exposure to solutions containing no glucose or to solutions containing 3-5 m M sodium azide the excitability of the terminals was not altered by the tetanus. After washing with the control solution, post-tetanic depression of excitability returned. Antimycin-A (1·8 × 10−6 M) had little or no effect upon post-tetanic excitability. 7. It was concluded that the post-tetanic depression of excitability reflected hyperpolarization of the terminals and that this hyperpolarization was caused by a shift of the membrane potential towards the potassium equilibrium potential because of an increase in potassium permeability.

55 citations


Journal ArticleDOI
TL;DR: The correlation of these data with electrical data on the same system (Weisenseel and Jaffe) and possible physiological consequences of the ion concentration changes are discussed.
Abstract: Intracellular ion concentrations were measured in the developing Pelvetia egg during the first 24 hr after fertilization. Intracellular K + and Cl − show large concentration increases during this period. Intracellular K + increases from 170 mmoles/liter at fertilization to 320 mmoles/liter at 8 hr and reaches 400 mmoles/liter by 24 hr. Intracellular Cl − increases from 87 mmoles/liter at fertilization to 194 mmoles/liter at 8 hr, and 320 mmoles/liter by 24 hr. Intracellular Na + shows smaller but significant concentration changes, increasing from 27 mmoles/liter at fertilization to 40 mmoles/liter at 8 hr, and then decreasing to 20 mmoles/liter at 24 hr. Neither Mg 2+ nor Ca 2+ vary significantly from 25 mmoles/liter and 4 mmoles/liter, respectively. The changes in Na + plus K + are approximately equal to the Cl − increase over the first 24 hr after fertilization but do not balance at every time interval. In agreement with the ion accumulation of the developing eggs is an increase of the intracellular osmotic pressure preceding germination. The correlation of these data with electrical data on the same system (Weisenseel and Jaffe) and possible physiological consequences of the ion concentration changes are discussed.

50 citations


Journal ArticleDOI
TL;DR: Frog (Rana pipiens) sciatic nerve was incubated, with and without stimulation, in an oil bath to study the correlation between changes in the magnitude of the compound action potential (α and β) and changes in metabolites, particularly energy reserves, during anoxia and recovery fromAnoxia.
Abstract: — Frog (Rana pipiens) sciatic nerve was incubated, with and without stimulation, in an oil bath. The correlation between changes in the magnitude of the compound action potential (α and β) and changes in metabolites, particularly energy reserves, during anoxia and recovery from anoxia was studied. The time to extinction of the action potential in anoxia was frequency-dependent. The action potential could not be restored, nor its extinction delayed, by washing the nerve in O2-free Ringer's solution. Therefore, in this system extracellular K+ accumulation was not a significant factor in blocking impulse conduction. At the time of complete nerve block resulting from anoxia (90 min at rest), ATP, P-creatine and glucose were 30, 10 and 10 per cent, respectively, of initial levels. Glycogen did not fall below 42 per cent of control levels even after 5 h of anoxia. Changes in the levels of energy reserves during anoxia were used to calculate the metabolic rate of nerves at rest and during stimulation. In one series of experiments, the resting metabolic rate was 0·12 mequiv. of ‘high-energy phosphate’ (∼P)/kg/min. Stimulation increased the metabolic rate to 0·22 mequiv. of ∼P/kg/min at 30 Hz and to 0·29 mequiv. of ∼P/kg/min at 100 Hz. The change in metabolic rate when the nerve passed from the resting to the stimulated state was quite abrupt, an observation suggesting that the slow transition observed with methods monitoring O2, consumption was largely instrumental. In nerve stimulated to exhaustion in the absence of O2, neither ATP nor P-creatine had fully recovered within 60 min after O2, was readmitted, although the action potential reached supranormal levels 15 min after return to O2. The ratio of lactate: pyruvate, which increased as expected during anoxia, paradoxically increased even further after O2, was readmitted. The rate of energy utilization during recovery was 0·30 mequiv. of ∼P/kg/min. Nerves stimulated at 100–200 Hz in O2, exhibited no changes in levels of P-creatine, ATP or lactate, an observation implying that the nerve could not be made to use ∼P faster than oxidation of glucose could provide it. This meant that the maximal metabolic rate was not limited by the rate of supply of chemical energy. Instead, the limitation may have arisen as a result of a limited rate at which ionic imbalance can result from stimulation or a limited pump capacity of the axonal membrane. Nerves stimulated at 200 Hz in O2 for 20 min and then transferred to an O2-free environment without further stimulation exhibited an increase in the rate of energy utilization (nearly two-fold) over the resting rate, a finding that suggested a metabolic (ionic?) debt as a result of activity which could not be met even though the energy supply was adequate. Therefore, restriction of energy expenditure by a limiting pumping rate seemed to be the most likely explanation. The resting metabolic rate of frog sciatic nerve was only one-quarter to one-third of the rate for rat sciatic nerve, when compared at the same temperature (25°C).

46 citations



References
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Book
31 Dec 1959
Abstract: This classic account describes the known exact solutions of problems of heat flow, with detailed discussion of all the most important boundary value problems.

21,797 citations




Journal ArticleDOI

37 citations


"Effects of azide and chloretone on ..." refers background or result in this paper

  • ...…have only slight metabolic effects on resting nerves (Brink, 1951), and narcotics are also known to affect the electrical resistance of frog muscle (Guttmau, 1939) and plant cells (Osterhout , 1922), dilute concentrations causing an initial increase in resistance that is followed by a decrease....

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  • ...These results are reminiscent of the experiments of Osterhout (1922) who showed that high concentrations of narcotics produced a progressive decrease in the electrical resistance of Laminaria agardkii....

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TL;DR: Reading studies from the rockefeller institute for medical research is also a way as one of the collective books that gives many advantages.
Abstract: No wonder you activities are, reading will be always needed. It is not only to fulfil the duties that you need to finish in deadline time. Reading will encourage your mind and thoughts. Of course, reading will greatly develop your experiences about everything. Reading studies from the rockefeller institute for medical research is also a way as one of the collective books that gives many advantages. The advantages are not only for you, but for the other peoples with those meaningful benefits.

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