Sodium efflux from voltage clamped squid giant axons.

Landowne, David

doi:10.1113/jphysiol.1977.sp011755

Cited by 6 publications

(6 citation statements)

References 25 publications

(43 reference statements)

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“…The stimulated extra Na influx, K efflux, and K influx are significantly greater in Myxicola than in squid (Table 4) and are therefore much closer to the theoretical values for squid predicted by the equations of Hodgkin and Huxley (1952, at 6~ cf, Cohen & Landowne, 1974;Landowne & Scruggs, 1976;Landowne, 1977). However, the agreement is probably fortuitous as net ionic currents during computed action potentials are several-fold lower in Myxicola than in squid (compare Goldman & Schauf, 1973;Goldman et al, 1975, to Hodgkin & Huxley, 1952.…”

Section: Resting and Stimulated Fluxes Of Na And Ksupporting

confidence: 66%

“…The Qlo ofNa efflux is greater than 3 below 5 ~ and less than 2 above 10 ~ Cohen and Landowne (1974) have reported that the extra Na influx and efflux associated with electrical activity has a Q10 near unity, in contrast to a Q10<0.5 predicted by Hodgkin and Huxley (1952). Recently Landowne (1977) has accounted for part of the discrepancy with the finding of a temperature-dependent component of Na efflux that requires external Na and therefore deviates from the principle of independence of unidirectional fluxes. In two experiments in which the temperature was raised from 5 to 10 or 17 ~ and then returned to 5 ~ the Qlo of stimulated Na efflux from Myxicola axons was only slightly different from 1.0 (Table 5B).…”

Section: Temperature Dependence Of Na Effluxmentioning

confidence: 85%

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Sodium and potassium fluxes across the dialyzed giant axon ofMyxicola

Forbush

1979

J. Membrain Biol.

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Resting and stimulated fluxes of sodium and potassium across the giant axon of the marine annelid, Myxicola infundibulum, have been characterized using the technique of internal dialysis. In most respects the ion movements were found to be similar to those in squid axons. Sodium efflux and potassium influx were found to be active, cardiac glycoside-sensitive fluxes, with a variable coupling ratio. However, when [ATP]i was lowered to less than 20 microM by treatment with cyanide and continuous dialysis, or to less than 2 microM by dialysis with glucose following injection of hexokinase, Na efflux and K influx were unaltered. The maintained fluxes were not accounted for by an increased passive permeability of the axolemma, although 30-60% of the Na efflux appeared to be due to Na-Na exchange. An altered form of Na pump operation at low [ATP]i is a more likely explanation than an alternate energy source, or an ATP source proximate to the axolemma. The transient response of 22Na efflux to a change in [22Na]i was found to be much slower than in squid, tau = 360 sec. The efflux delay could only be accounted for by an extra-axonal diffusion barrier, which is probably the basement membrane surrounding the ventral nerve cord.

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Section: Resting and Stimulated Fluxes Of Na And Ksupporting

confidence: 66%

Section: Temperature Dependence Of Na Effluxmentioning

confidence: 85%

Sodium and potassium fluxes across the dialyzed giant axon ofMyxicola

Forbush

1979

J. Membrain Biol.

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“…Because of the Na/K pump action, it is mainly intracellular, though it flows extracellularly during cell membrane repolarization [43,55]. Moreover, its transmembrane movement is related to H + movement, in the regulation of blood pH, and to cell volume [1,56,57]. Therefore, an increase in serum K concentration may be due to morphofunctional membrane alteration, cell lysis, in particular hemolysis, inorganic acidosis, and renal insufficiency or failure [1,56].…”

Section: Discussionmentioning

confidence: 99%

Exploratory Factor Analysis of Rainbow Trout Serum Chemistry Variables

Manera

2021

IJERPH

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Clinical chemistry offers a valuable, affordable, moderately invasive, and nondisruptive way to assess animal physiological status and wellness within defined ranges and is widely used as a diagnostic clinical tool. Because of physiological differences between mammals, clinical correlates of blood chemistry variables are not known in detail in fish, in which tissue/organ function tests are inferred from mammal-derived clinical chemistry data. The aim of the present study was to apply exploratory factor analysis on a serum chemistry dataset from clinically healthy, reared rainbow trout Oncorhynchusmykiss (Walbaum, 1792) to select the most correlated variables and to test for possible underlying factors explaining the observed correlations as possible physiological status estimates in trout. The obtained factors were tested for correlation with hepatosomatic and splenosomatic indexes. Thirteen highly correlated variables were selected out of 18 original serum chemistry variables, and three underlying factors (Factors 1, 2, and 3) were identified that explained the observed correlations among variables. Moreover, Factor 1 correlated negatively with the hepatosomatic index and Factors 2 and 3 negatively with the splenosomatic index. The obtained factors were tentatively associated with: protein (liver) metabolism (Factor 1), cell turnover (Factor 2), and lipid (muscle) metabolism (Factor 3).

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“…Such an increase was never seen, even at low initial quantal contents. A final reason for suspecting that temperature-dependent changes in Ca2+ influx do not account for the temperature sensitivity of evoked release is that in squid axons the action potential-dependent Ca2+ and Na+ influxes actually decrease with increasing temperature (Hodgkin & Keynes, 1957;Landowne, 1977). Thus although the evidence is indirect, it appears that the temperature sensitivity of evoked release is due mainly to changes in rate-limiting steps other than Ca2+ influx.…”

Section: Discussionmentioning

confidence: 99%

“…The synaptic delay would not be expected to change if the temperature jump merely increased Ca2+ influx, because the minimal synaptic delay is not sensitive to extracellular [Ca 2+] (Katz & Miledi, 1965b). A second reason is based on Katz & Miledi's (1968) (Hodgkin & Keynes, 1957;Landowne, 1977). Thus although the evidence is indirect, it appears that the temperature sensitivity of evoked release is due mainly to changes in rate-limiting steps other than Ca2+ influx.…”

Section: Discussionmentioning

confidence: 99%

Temperature‐sensitive aspects of evoked and spontaneous transmitter release at the frog neuromuscular junction.

Barrett

Botz

et al. 1978

The Journal of Physiology

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SUMMARY1. The temperature dependence of presynaptic processes involved in neuromuscular transmission was studied by rapidly increasing the temperature of cooled frog neuromuscular junctions by 4-10 0C using pulses from a neodymium laser. The temperature elevation was complete within 0 5 msec, and decayed back to control levels with a time constant of about 7-8 sec.2. Temperature jumps completed before nerve stimulation increased the quantal content and decreased the latency of the end-plate potential (e.p.p.). The Q10 for

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Sodium efflux from voltage clamped squid giant axons.

Cited by 6 publications

References 25 publications

Sodium and potassium fluxes across the dialyzed giant axon ofMyxicola

Sodium and potassium fluxes across the dialyzed giant axon ofMyxicola

Exploratory Factor Analysis of Rainbow Trout Serum Chemistry Variables

Temperature‐sensitive aspects of evoked and spontaneous transmitter release at the frog neuromuscular junction.

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