bluuebunny/crossref_metadata_2025_split huggingface dataset:
A study of frog muscle maintained in organ culture
Authors: Harris A. J. , Miledi R. 
Published: December 2014

1. Frog muscles are isolated and maintained in organ culture conditions for periods of up to 2 months. During the first 2 weeks, muscle fibres have normal resting membrane and action potentials. Subsequently the potentials decline in amplitude.2. Slow muscle fibres also survive in culture and retain their ability to give maintained contractures.3. Muscle sensory receptors continue to function in culture until the axon terminals degenerate at about 2 weeks.4. Neuromuscular transmission is normal during the first few days of culture, after which the motor endings degenerate. Transmission persists longer (up to 17 days) if a long segment of nerve is left attached to the muscle. With short‐nerve preparations failure of transmission in vivo occurs at about the same time as in culture. With long‐nerve preparations failure of transmission is delayed even further in culture.5. In short‐nerve preparations miniature end‐plate potentials disappear, in general, at about the time that transmission fails. In long‐nerve preparations some end‐plates continue to have miniature end‐plate potential activity for a short time after nerve impulses cease to evoke any response; but eventually miniature potential activity disappears from all end‐plates.6. After a few days of electrical silence, miniature end‐plate potentials reappear at some of the denervated end‐plates. The proportion of denervated end‐plates which show miniature end‐plate potentials in culture is smaller than in muscles denervated in situ.7. Electron microscopy shows that muscle structure is well preserved in culture, that the axons degenerate and that the Schwann cells move to occupy the space vacated by the axons. The Schwann cells are very probably the source of the acetylcholine which evokes miniature potentials in the denervated end‐plates.
The transport of L‐leucine in human erythrocytes: a new kinetic analysis
Authors: Hoare D. G. 
Published: December 2014

1. Data on the transport of
L‐leucine into human erythrocytes at 25° C shows (a) that the carrier re‐orientation process is rate determining, (b) that the binding of leucine to the carrier increases the rate of carrier re‐orientation and (c) that the carrier is, at equilibrium, about equally distributed between the membrane surfaces at 25° C.2. These conclusions are reached through a new kinetic analysis of a simple carrier system, which involves no prior assumptions about the relative magnitudes of the rate constants, yet leads to usable kinetic equations. These equations allow the determination of the rate determining step, the calculation of the effect of bound substrate on the rate of carrier re‐orientation and, in some cases, an estimate to be made of the equilibrium distribution of the carrier between the inner and outer membrane surfaces.
The temperature dependence of the transport of L‐leucine in human erythrocytes
Authors: Hoare D. G. 
Published: December 2014

1. Experiments are reported on the entry, exit and exchange fluxes of
L‐leucine in human erythrocytes in the temperature range 0–37° C. The kinetics of entry and exit become quite different at low temperatures, indicating an asymmetry in the transport mechanism.2. The data is analysed in terms of a simple carrier mechanism. This shows that carrier re‐orientation is rate determining at all temperatures studied, and suggests, although does not prove, that the origin of the asymmetry of the carrier may be an unequal equilibrium distribution of the carriers between inward and outward orientations.3. The activation energy increases sharply on going to low temperatures. This increase is the sum of two components. One arises from differences between the activation energies for inward and outward carrier re‐orientations, and the other from changes, with temperature, in the activation energies of the individual carrier re‐orientation steps.
Accumulation and apparent active transport of prostaglandins by some rabbit tissues in vitro
Authors: Bito L. Z. 
Published: December 2014

1. Slices or bits of rabbit tissues, not exceeding 100 mg, were incubated in tissue culture medium containing tritium‐labelled prostaglandin ([3H]PG). In some experiments, incubation medium also contained saturating concentrations of an unlabelled prostaglandin (PG), or [14C]‐sucrose for determination of extracellular space. At the end of the incubation period, usually 1 hr, the tissues were removed and weighed, and their 3H (and 14C) content were determined along with that of a unit volume of medium.2. Tissues known to play a central role in PG metabolism (lung and liver) and in its excretion (kidney cortex) and tissues which have a known function in blood‐brain and blood‐ocular barriers (choroid plexuses and ciliary processes) show a large accumulation of 3H when incubated in a medium containing [3H]PGE1. In addition, tissues of the female reproductive tract, and the aorta of the rabbit show similar 3H accumulation. When uncorrected for tissue solid content or extracellular water volume, the extent of this accumulation is two‐ to sixfold. Calculated on the basis that all excess 3H is present in the free form in the intracellular water, the accumulation ratio for ciliary processes, for example, indicates an over fortysix‐fold gradient of PGE1 across the cell membrane.3. Tissues which accumulate [3H]PGE1 also accumulate [3H]PGA1, [3H]PGF1α and [3H]PGF2α. In some tissues specificity is, however, apparent; in the lung accumulation of [3H]PGA1 was significantly greater than that of [3H]PGF1α.4. The extent of [3H]PGE1 accumulation was decreased, or in some tissues completely inhibited, by incubation at 2° C, or by addition of large concentrations of unlabelled PG.5. Accumulation of [3H]PGE1 by the foetal liver is not apparent on the 20th day of gestation, but is fully developed by the 30th day of gestation. The foetal lung does not accumulate [3H]PGE1 at any stage of gestation.6. In some tissues, most notably muscle, there appears to be full equilibrium of [3H]PGE1 between tissue water and medium within 1 hr of incubation.7. PGs are partially excluded from the intracellular volume of some other tissues, most notably the spleen and subcutaneous connective tissues. This apparent exclusion cannot be blocked by incubation in the cold, or by the addition of saturating levels of unlabelled PG.8. The simplest explanation for all observed results is that cell membranes are, in general, impermeable to PGs. However, there are specific, carrier‐mediated mechanisms across some membranes which facilitate the entry of PGs. In some cells these transport mechanisms are linked to a source of metabolic energy, and/or to the counter‐transport of some other substance, thus allowing net accumulation of PGs against a concentration gradient. Alternatively, 3H accumulation may represent adsorption of [3H]PGs or one of their labelled metabolites on to specific adsorption sites.
An investigation of sodium transport in barnacle muscle fibres by means of the microsyringe technique
Authors: Bittar E. Edward , Chen Stephen , Danielson Bo G. , Hartmann Henrik A. , Tong Edmund Y. 
Published: December 2014

1. The cation composition of single barnacle muscle fibres following damage by axial insertion of a microsyringe has been measured. The Na and Ca contents of these fibres were raised.2. Electronmicroscopic studies of fibres following insertion of a microsyringe indicated that the damage done resulted in tubular obstruction of the T‐system.3. Fibres loaded with radiosodium by micro‐injection showed that the Na* efflux declined exponentially with time, but that in most fibres the slope ratio of d/dt ln [Na*]1 to d/dt (ln d[Na*]i/dt) was less than unity. Injections of distilled water deep in the fibre failed to influence the course of the Na* efflux.4. K removal reduced the Na efflux by 47%. However, a few fibres displayed very little K‐dependence.5. When measured in fibres already soaked in a K‐free medium for long periods the sodium efflux consisted of a brief rapid phase, followed by a slow phase of Na loss.6. In the presence of 30 m
M‐K, there was little or no rise in the Na efflux. Raising the external K to 50 or 100 m
M caused a marked rise in the Na efflux. Raising the external K to 30 m
M in the absence of external Ca2+ led to a rise in the Na efflux. A high K solution always caused shortening of these fibres.7. Internal application of 1
M or 1 m
M‐CaCl2 often caused a significant rise in the Na efflux.8. Internal application of 2·5 or 5
M saline caused a prompt and large fall in the Na efflux. In the presence of high K saline‐loaded fibres failed to contract.9. Internal application of 0·5
M‐ATP stimulated the Na efflux. A larger effect was not observed in fibres pre‐treated with 2
M‐MgCl2. Internal application of 0·5
M‐ArP was without effect.10. The results indicate that the barnacle fibre is a suitable preparation for the study of Na fluxes by means of the micro‐injection technique. They also indicate that the mechanism regulating the Na efflux is not quite the same as that found in squid axon or frog muscle.
Some properties of the presynaptic nerve terminals in a mammalian sympathetic ganglion
Authors: Dunant Y. 
Published: December 2014

1. Superior cervical ganglia of adult rats were excised and maintained in vitro in stable conditions. Potentials were recorded with external electrodes. After transmission was blocked by mecamylamine, a small potential change was recorded from the rostral area of the ganglion in response to preganglionic stimulation.2. This electrical response was identified as the presynaptic action potential recorded from the nerve terminals by a number of criteria based on histological and physiological considerations including the disappearance of the spike in a glucose free solution. As shown by Nicolescu, Dolivo, Rouiller & Foroglou‐Kerameus (1966) on the same preparation this condition causes an irreversible and selective lesion of the presynaptic nerve endings.3. A suitable concentration of mecamylamine permitted the presynaptic response and the excitatory post‐synaptic potential (EPSP) to be recorded simultaneously. As the stimulus was increased, the EPSP increased linearly with the amplitude of the presynaptic response.4. After replacement of potassium ions in the bathing solution by caesium and during the early phase of post‐tetanic facilitation there was an increase in the presynaptic response accompanied by a disproportionate increase in the EPSP.5. No changes in the presynaptic response were found in the presence of the following drugs, all of which depressed the EPSP: acetylcholine, hemicholinium, curare, further doses of ganglion‐blocking agents, and high Mg2+ and low Ca2+ concentrations.6. Ouabain (4·5 × 10−4
M) reversibly decreased the amplitude of the presynaptic response and increased the spontaneous release of transmitter. The EPSP was at first enhanced and then depressed.
Modification of the evoked release of noradrenaline from the perfused cat spleen by various ions and agents
Authors: Kirpekar S. M. , Prat J. C. , Puig Margarita , Wakade A. R. 
Published: December 2014

1. Cat spleens were perfused with Krebs‐bicarbonate solution at a rate of about 7 ml./min at 33–35° C. Noradrenaline release after splenic nerve stimulation at 10 or 30 Hz was measured. Effects of various ions and drugs on noradrenaline release were determined.2. Perfusion of phenoxybenzamine‐ and [3H]noradrenaline‐treated spleens with 1, 2·5 and 5 m
M cobalt or nickel—2 Krebs solution markedly reduced the release of noradrenaline by nerve stimulation. Lanthanum was the most potent inhibitor of noradrenaline release. Increasing the calcium concentration or adding tetraethylammonium chloride (TEA) partially counteracted the inhibitory effects of cobalt on release. Cobalt did not inhibit release induced by tyramine.3. Calcium did not cause spontaneous release of noradrenaline either when high concentrations were injected directly into the spleen or after first perfusing the spleen with calcium‐free medium.4. Carbachol, protoveratrine and high potassium inhibit, whereas TEA, barium and rubidium enhance, the evoked release of noradrenaline.5. The relation of noradrenaline release to influx of calcium ions and its modification by various agents has been discussed.
Peritubular pH and transtubular potentials in isolated perfused cortical collecting ducts of rabbit kidney
Authors: Douglas R. J. , Isaacson L. C. 
Published: December 2014

1. Cortical collecting ducts were dissected from slices of rabbit kidney, then perfused in vitro.2. Transtubular electrical potentials were measured before and after abrupt changes in peritubular fluid pH.3. Variation in peritubular fluid pH, induced either by alteration in HCO3− concentration or in H2PO4−/HPO42- ratio, produced biphasic responses in potential. Thus, reduction in pH caused an immediate fall, and then a prolonged and marked rise, in transtubular potential. The converse occurred on raising the pH.4. Variation in luminal fluid pH between pH 4·85 and pH 7·35 did not alter this pattern of response.5. In contrast to the above, reduction of peritubular fluid pH by elevation of pCO2 produced either no effect or a decrease in transtubular potential.6. The transtubular potential of the cortical collecting duct appears to be a function of the pH gradient across some as yet unidentified part of the wall of the duct.
Excitation and inhibition of motoneurones in the tortoise
Authors: Rosenberg M. E. 
Published: December 2014

1. Intracellularly recorded responses of lumbosacral motoneurones in the tortoise are described. The preparation was decerebrate and unanaesthetized. Cells were tested by stimulation of the main branches of the ipsilateral sciatic nerve.2. The distribution of cells according to resting membrane potential is given; highest recorded values were around 70 mV.3. The action potential has a step on the rising phase and has a total duration in the region of 4 msec.4. The motoneurone input resistance, measured by the spike height method, was 5‐8 MΩ.5. Orthodromic excitation of motoneurones occurred after a central latency of 2 msec.6. Inhibition, and inhibitory (hyperpolarizing) potentials were demonstrated. Peak amplitude of maximum response was frequently greater than 10 mV. The potentials were influenced by injected currents in a manner resembling IPSPs in mammalian motoneurones. Minimum central latency for inhibitory potentials was about 3 msec.7. Membrane potentials and dimensions of action potentials for motoneurones in the cat are given for purposes of comparison with the tortoise.
Inhibition of denervation changes in skeletal muscle by blockers of protein synthesis
Authors: Grampp W. , Harris J. B. , Thesleff S. 
Published: December 2014

1. A study was made of the effects of inhibitors of protein synthesis (actinomycin D, chloramphenicol and cycloheximide) on the in vivo development of extrajunctional cholinergic receptors, tetrodotoxin‐resistant action potentials, slowing of the time course of the action potential, and on the fall in the resting membrane potential in denervated mouse skeletal muscle.2. Actinomycin D (0·5 mg/kg,
I.P.) reduced the incorporation of uridine into skeletal muscle by 50–60% for 4‐5 days. There was no simultaneous reduction in
L‐leucine incorporation.3. Actinomycin D (0·5 mg/kg
I.P., 1 day after denervation) inhibited the development of extrajunctional cholinergic receptors, tetrodotoxin‐resistant action potentials and the fall in resting membrane potential for approximately 4 days.4. The post‐denervation fall in the maximum rate of rise and in the amplitude of the overshoot of the muscle fibre action potential was unaffected by actinomycin D treatment.5. Actinomycin D failed to inhibit the appearance of the membrane changes if given later than 2 days after denervation.6. Chloramphenicol (6 g/kg in divided doses) and cycloheximide (40 g/kg every 12 hr) were also able to inhibit the appearance of the membrane changes.7. It is concluded that some denervation induced changes in the muscle fibre membrane depend on the synthesis of new proteins. The results imply that the motor nerve cell normally exerts a regulatory influence on the genome of the muscle cell.
The effect of external anions on steady‐state chloride exchange across ascites tumour cells
Authors: Aull Felice 
Published: December 2014

1. The rate of cell chloride exchange, or efflux coefficient, was measured after equilibration in media of different anionic composition.2. When sulphate substituted for chloride in the medium, the efflux coefficient was always higher than in control chloride solutions and varied inversely with external chloride concentration. In sulphate the chloride efflux coefficient varied from 19·6 to 100·7 hr−1. The mean control efflux coefficient was 6·60 ± 0·677 (
S.E. of mean).3. In contrast, when external nitrate substituted for chloride, the efflux coefficient was independent of external chloride concentration and the same as in control chloride media. The mean value in nitrate was 6·42 ± 0·603 (
S.E. of mean). The results confirm findings of Hempling & Kromphardt (1965).4. Steady‐state chloride flux varied in direct proportion to the external chloride concentration, which would be expected for passive chloride exchange. However, the slope of the line relating these variables was higher in sulphate than in nitrate and control media. Thus at any given external chloride concentration chloride flux was greater in sulphate than in nitrate and control solutions.5. It is suggested that the effect of sulphate to increase cell chloride exchange may be related to its greater tendency to bind water, relative to chloride and nitrate.
Ion transport across an isolated preparation of sheep rumen epithelium
Authors: Ferreira H. G. , Harrison F. A. , Keynes R. D. , Zurich L. 
Published: December 2014

1. The fluxes of isotopically labelled sodium, potassium and chloride passing in each direction across isolated sheets of rumen epithelium from the sheep have been measured under short‐circuit conditions.2. With both sides of the epithelium bathed in chloride Ringer the mean sodium fluxes were 2·85 μmole/cm2.hr from rumen to blood and 1·28 μmole/cm2.hr in the reverse direction. In sulphate Ringer the sodium fluxes were 1·64 μmole/cm2.hr from rumen to blood and 0·54 μmole/cm2.hr from blood to rumen.3. In chloride Ringer the mean potassium fluxes were 0·18 μmole/cm2.hr from rumen to blood and 0·54 μmole/cm2.hr from blood to rumen. In sulphate Ringer the potassium fluxes were 0·07 μmole/cm2.hr from rumen to blood and 0·35 μmole/cm2.hr from blood to rumen.4. In chloride Ringer the mean chloride fluxes were 4·89 μmole/cm2.hr from rumen to blood and 3·78 μmole/cm2.hr from blood to rumen.5. In chloride Ringer the mean value of the short‐circuit current was 13 μA/cm2, corresponding to a flux of 0·49 μequiv/cm2.hr. When sulphate was substituted for chloride, the short‐circuit current was increased by about 40%, and the net flux of sodium from rumen to blood fell by 30%.6. Neither the sodium nor the chloride fluxes changed significantly when the epithelium was temporarily open‐circuited.
Changes in the intestinal transport of sodium induced by exposure of goldfish to a saline environment
Authors: Ellory J. C. , Lahlou B. , Smith M. W. 
Published: December 2014

1. The uptake and transflux of sodium by goldfish intestines has been compared under different experimental conditions. Uptake was measured from a 1 min contact of the intestinal mucosa with radioactive sodium chloride solution. Transflux was measured over a period of 2 hr using the everted sac technique.2. Keeping goldfish in saline reduced the transflux of sodium to one quarter the value found for fresh‐water fish. The uptake of sodium was halved by this treatment. Cortisol injected previously into saline‐adapted fish changed neither the transflux nor the uptake of sodium measured subsequently.3. In fresh‐water fish hypophysectomy reduced sodium transflux while leaving the uptake of sodium unchanged. Injection of cortisol restored sodium transflux to control levels without producing any additional effects on the uptake of sodium.4. It is suggested that adaptation to saline involves regulation of sodium movement across the microvillar membrane of the mucosal cell. Cortisol would appear to play no part in this type of regulation.5. The presence of cortisol, or possibly other steroids with similar actions, has however been shown to be essential for the normal operation of sodium transport in this tissue. It is not clear exactly how cortisol exerts this effect. What evidence there is suggests that cortisol exerts a metabolic control rather than changing directly the membrane permeability of the cell.
Intracellular calcium movements in skinned muscle fibres
Authors: Ford L. E. , Podolsky R. J. 
Published: December 2014

1. Force development and 45Ca movement between the internal membranes and the myofilament space were measured in segments of skinned muscle fibres.2. At 20° C calcium ions in the myofilament space of calcium loaded fibres caused the internal membranes to release a substantial amount of calcium which produced a large force spike. Calcium produced a similar force spike in fibres containing only the physiological level of calcium when the temperature was lowered to about 6° C.3. The force spike at 6° C was inhibited when the magnesium concentration in the bathing solution was increased from 1 to 6 m
M. The pattern of force development in preparations transferred directly from oil to a free calcium solution indicated that the normal concentration of Mg2+ in the myofilament space of intact fibres is of the order of 10−3
M.4. A possible role for the regenerative calcium release mechanism in the physiological activation of muscle fibres is suggested.
The effect of voltage on the time course of end‐plate currents
Authors: Magleby K. L. , Stevens C. F. 
Published: December 2014

1. End‐plate currents have been studied in glycerol‐treated frog sartorius nerve—muscle preparations with the voltage clamp technique.2. End‐plate currents follow a simple exponential time course over most of their declining phase.3. The rate constant α that characterizes this exponential decay depends upon membrane potential V according to the relationship α (V) = BeAV, with A = 0·00795 ± 0·00043 (
S.E.) mV−1 and B = 1·67 ± 0·04 (
S.E.) msec−1.4. Voltage sensitivity decreases (that is, A in the above equation becomes smaller) as the recording and current‐passing electrodes are moved away from the end‐plate region.5. The voltage sensitivity of α is decreased by decreasing the gain of the voltage clamp amplifier.6. Changing the end‐plate current amplitude by curare treatment, by increased calcium ion concentration, and by facilitation and depression has essentially no effect on end‐plate current time course.7. When membrane potential is changed step‐wise during the decaying phase of the end‐plate conductance change, currents begin to decline with a rate constant α appropriate to the new membrane potential in less than 0·2 msec.8. Treatment with prostigmine methylsulphate in concentrations up to 50 μg/ml. slows end‐plate current decay but has little effect on voltage sensitivity. That is, B in the above equation is decreased by prostigmine treatment, but A is relatively unaffected.