bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of the performance of work on total energy output and metabolism during muscular contraction
Authors: Curtin Nancy A. , Gilbert Claude , Kretzschmar K. M. , Wilkie D. R. 
Published: December 2014

1. The production of heat (h) and work (w) and the changes in phosphocreatine (PCr) and ATP have been measured on tetanized isolated frog muscles (unpoisoned and in oxygen at 0° C) during shortening at constant velocity and during isometric contraction (both without relaxation). The former type of contraction was designed to maximize the fraction w/(h + w); the latter to minimize it.2. The duration of the isometric contraction was made considerably longer than that of the isovelocity contraction so that the (h + w) productions during the two contractions were approximately equal.3. The PCr break‐down during the working contraction was considerably greater than that during the isometric contraction.4. No detectable ATP changes occurred.5. The break‐down of PCr is sufficient to account for the work evolved: there is no reason to suppose that the work comes from an unidentified source.6. In both types of contraction extra energy is evolved that cannot be accounted for by concurrent splitting of PCr. The time course of evolution of this extra energy is similar in all types of contraction, suggesting that it may arise from a process other than cross‐bridge interaction.7. The results are discussed in terms of current cross‐bridge theory and muscle kinetics. The mean cycle times of a cross‐bridge during working and isometric contractions are 0·12 sec and 0·34 sec respectively. During the working contraction cross‐bridges spend about one quarter of the time attached to actin filaments.
Degeneration secretion of saliva in the rat following sympathectomy
Authors: Delfs Ursula , Emmelin N. 
Published: December 2014

1. After previous extirpation of the superior cervical ganglion saliva was found to flow from the cannulated submaxillary duct of rats under chloralose anaesthesia. The secretion started 13–14·5 hr after sympathectomy, increased gradually in rate and then slowed down and ceased, lasting for about 12 hr.2. Injection of α‐ or β‐adrenoreceptor blocking drugs reduced the flow and a combination of both types of drugs abolished it. It is concluded that the secretion was caused by noradrenaline released from the degenerating nerves, and that the phenomenon is an example of the degeneration activity described in other preparations as an effect of section of post‐ganglionic autonomic nerves.3. A similar, but less pronounced, secretion was found in the parotid gland of the rat.
The effect of glucagon on the liver cell membrane potential
Authors: Petersen O. H. 
Published: December 2014

1. Intracellular recordings of membrane potential were made from superficial cells of isolated mouse liver segments superfused with physiological salt solutions.2. The mean resting cell membrane potential was −39·4 mV.3. Glucagon caused a dose‐dependent membrane hyperpolarization which was detectable at 10−9
M and maximal (7 mV) at 10−7
M. The hyperpolarization started within half a minute after exposure to glucagon. Secretion (2 × 10−7
M) had no effect on the membrane potential.4. Adrenaline (10−6
M) and isoprenaline (10−6
M) also caused membrane hyperpolarization (4–6 mV). The effect of isoprenaline, but not that of adrenaline, was blocked by propranolol (5 × 10−6
M).5. Dibutyryl adenosine 3′,5′‐monophosphate (10−3
M) caused a membrane hyperpolarization of 4–8 mV.6. In the absence of extracellular K or the presence of Strophanthin‐G (10−3
M) the resting potential was decreased and the response to glucagon reduced. During exposure to a solution containing 20 m
M‐K the resting potential was slightly enhanced and the amplitude of the glucagon‐induced hyperpolarization reduced compared with control conditions.7. It is concluded that the effect of glucagon on the membrane potential is due to an interaction with specific membrane receptors probably leading to activation of the membrane‐bound adenyl cyclase. It is probable that the hyperpolarization is mediated by cyclic AMP. The hyperpolarization induced by glucagon is dependent on a normal function of the membrane Na—K pump.
The morphological types of ganglion cells of the domestic cat's retina
Authors: Boycott B. B. , Wässle H. 
Published: December 2014

1. Three distinct morphological types of cat retinal ganglion cells have been identified and categorized as α, β and γ. Alpha ganglion cells have dendritic field diameters from 180 to 1000 μm; β, about 25 to 300 μm; γ, 180 to 800 μm, possibly more.2. The dimensions of the α and β ganglion cell dendritic fields increase monotonically from the central area outwards to the periphery; those of the γ cells do not. Seemingly a spectrum of sizes of the γ cells is found at most locations in the retina.3. All three morphological types of ganglion cells are found in the central area.4. Possible further anatomical types of ganglion cells are discussed. Correlations are suggested between the morphological category α cells and the physiological class Y cells; between β cells and the X cells and between the γ cells and the W cells.
Chronic effects of botulinum toxin on neuromuscular transmission and sensitivity to acetylcholine in slow and fast skeletal muscle of the mouse
Authors: Tonge D. A. 
Published: December 2014

1. A sublethal dose of botulinum toxin (type A) was injected into the muscles of one hind limb of the mouse causing local paralysis.2. Neuromuscular transmission and muscle sensitivity to acetylcholine (ACh) were studied in vitro in soleus and extensor digitorium longus (EDL) from 6 hr to 4 months after the injection of toxin.3. Both soleus and EDL failed to respond to nerve stimulation within 6 hr of the injection of toxin.4. In muscle fibres in which neuromuscular transmission was blocked, subthreshold end‐plate potentials (e.p.p.s) were recorded. The amplitude of the e.p.p.s increased during recovery from the effects of the toxin and both muscles contracted in response to nerve stimulation after 2‐3 weeks.5. For about 2 months muscles fatigued more rapidly than normal during repetitive nerve stimulation because of the low quantal content of e.p.p.s.6. Supersensitivity to ACh developed in 3‐5 days and persisted after the return of neuromuscular transmission. Muscle sensitivity to ACh became normal when the rate of fatigue during nerve stimulation was normal.
Calcium release in relation to permeability changes in toad bladder epithelium following antidiuretic hormone
Authors: Cuthbert A. W. , Wong P. Y. D. 
Published: December 2014

1. Methods for measuring the release of 45Ca from isolated urinary bladders of toads (Bufo marinus) pre‐loaded with this isotope have been devised. One method allowed separate collection from the mucosal and serosal surfaces of the bladders.2. Reducing the ambient calcium concentration reduced the rate of 45Ca efflux suggesting that efflux of radiolabel represents calcium exchange.3. Antidiuretic hormone, theophylline and prostaglandin E1 all increased calcium efflux, while lanthanum and amphotericin were without effect. Cyclic AMP caused only an inhibition of calcium release.4. The increase in 45Ca efflux due to antidiuretic hormone came exclusively from the mucosal side. Experiments with EGTA suggest that the calcium entering the mucosal solution arises mainly from superficial sites in the mucosal membrane.5. The release of 45Ca by hormone was not influenced by removal of sodium from the bathing solution. Low pH and amiloride reduced or abolished calcium release to hormone.6. The time course of calcium release from the mucosal surface due to hormone was rapid (commencing between 0·5 and 1·5 min after hormone application). Thus calcium release precedes the increase in sodium transport and hydro‐osmotic flow following hormone, and appears to be at least as rapid as cyclic AMP generation in the tissue.7. The relationship between calcium release or exchange and the permeability changes in the bladder to water and to sodium, following hormone, are discussed.
The sensitivity to glutamate of denervated muscles of the crayfish
Authors: Frank Eric 
Published: December 2014

The effect of denervation on the sensitivity of muscle fibres to glutamate was studied in leg muscles of crayfish.1. When the motor nerve was cut close to the proximal accessory flexor muscle the distal end of the nerve degenerated. Neuromuscular transmission failed and spontaneous miniature potentials disappeared after two months. Several stages of nerve terminal degeneration were seen in muscles denervated between 1 and 3 months, and after 4 months no remains of synapses could be found.2. Following denervation for periods up to 8 months there was no significant change in sensitivity to glutamate, a substance that mimics the action of the neural transmitter. Depolarizations produced by various concentrations of glutamate in the bathing solution were the same in denervated and control muscle fibres. Moreover, the sensitivity to iontophoretically applied glutamate was localized to discrete patches as in innervated muscles.3. Supersensitivity of muscles apparently does not occur after denervation in the crayfish.
Localization of beta adrenergic receptors, and effects of noradrenaline and cyclic nucleotides on action potentials, ionic currents and tension in mammalian cardiac muscle
Authors: Reuter H. 
Published: December 2014

1. Isoprenaline and noradrenaline were applied iontophoretically to cardiac Purkinje fibres. Intracellular application of the drugs had no effect, while extracellular application of the same amounts of charge caused acceleration of pace‐maker activity and a shift of the plateau level of the action potential. These results indicate that β‐adrenergic receptors are located at the outside of the cardiac cell membrane.2. A systematic comparison of the effects of cyclic AMP derivatives and noradrenaline on action potentials and isometric tension of ventricular myocardial preparations showed that the nucleotides and the catecholamine increase the plateau height and the duration of the action potential and also increase tension. However, there are quantitative differences in the action of these drugs.3. Cyclic AMP derivatives and noradrenaline increase the slow inward current, ICa, in ventricular myocardial preparations. Voltage clamp analysis of ICa showed that the kinetic parameters of this membrane current are not affected by these drugs. However, the membrane conductance to Ca ions is greatly increased by noradrenaline and to a smaller extent by dibutyryl cyclic AMP.4. Concentration—response relations of the membrane effects of noradrenaline on plateau height of the action potential and on ICa could be fitted by the same theoretical log concentration—response curve. The Hill plot of this concentration—response curve had a slope of 2. The half maximal response occurred at 5 × 10−7
M.5. The results are compared with other membrane effects of catecholamines and cyclic nucleotides in cardiac muscle. The effects on ICa are related to the positive inotropic effect of the drugs.
Transport of rubidium and sodium in pancreatic islets
Authors: Sehlin J. , Täljedal I.‐B. 
Published: December 2014

1. Fluxes of 86Rb+ and 22Na+ were measured in pancreatic islets of ob/ob‐mice. The islets, which contain more than 90% β‐cells, were incubated at 37° C in Krebs—Ringer bicarbonate buffer with modifications known to influence insulin release.2. In the presence of Na+, the islets vigorously accumulated Rb+. The Rb+ uptake was inhibited by depletion of islet Na+ or by 1 m
m ouabain or 0·1 m
m chloromercuribenzene‐p‐sulphonic acid. Rb+ uptake was stimulated by 1 m
m‐5,5′‐dithiobis (2‐nitrobenzoic acid) or by depletion of islet Ca2+, while 20 m
m glucose, 5 m
m theophylline, 0·1 m
m iodoacetamide, or 1 m
m‐6,6′‐dithionicotinic acid had no significant effects.3. The efflux of Rb+ from preloaded islets followed exponential kinetics with a half‐life of about 16 min. The rate of efflux was enhanced by 0·1 m
m chloromercuribenzene‐p‐sulphonic acid and inhibited by 20 m
m glucose. Omission of Na+, K+ or Ca2+ from the incubation medium had no significant effects.4. The efflux of 22Na+ from islets preloaded with this isotope was enhanced by 0·1 m
m chloromercuribenzene‐p‐sulphonic acid or by Ca2+ deficiency. It was inhibited by 1 m
m ouabain, 0·1 m
m‐2,4‐dinitrophenol, or by omission of Na+ from the incubation medium. Omission of K+ or the addition of 20 m
m glucose had no significant effects.5. It is concluded that the β‐cells are permeable to Na+ and Rb+ and expel Na+ by an active mechanism similar to, or identical with, the Na+/K+‐pump in other cells. The mechanisms of active and passive cation movements are discussed in relation to current hypotheses of stimulus‐secretion coupling in the β‐cells depending on interactions between Na+ and Ca2+. In particular, the results support the hypotheses of insulin release being stimulated by ouabain through inhibition of the Na+/K+‐pump and by organic mercurials through enhancement of membrane permeability to cations.
Electrical responses of double cones in the turtle retina
Authors: Richter Amrei , Simon E. J. 
Published: December 2014

1. Responses to monochromatic flashes were recorded intracellularly from double cones in the retina of the turtle, Pseudemys scripta elegans. Double cones have been identified by intracellular marking with Procion Yellow dye.2. The direct light response of a double cone is a hyperpolarization graded with the intensity of a flash and similar to the response of single cones.3. When flashes were dim, responses were proportional to light intensity but varied in time course as a function of wave‐length. They reached peak in about 120 msec for deep red stimuli and about 143 msec for green stimuli.4. When applied over red backgrounds, responses to red flashes became smaller, faster and frequently diphasic, but responses to green remained similar to those recorded from darkness. Green backgrounds made responses to all colours small and fast.5. Linear spectral sensitivity curves have peaks corresponding to the peak sensitivities of single red‐sensitive and green‐sensitive cones. Red and green backgrounds suppressed red and green sensitivity respectively.6. Large fields of illumination evoked composite responses which included the direct light response, its enhancement from illumination of nearby receptors and the depolarizing effect of luminosity horizontal cell impingement. In the green‐sensitive element the depolarizing effect was larger for red than for green flashes, and stimulation with red annuli evoked net depolarizing responses.7. It is concluded that the responses of double cones may be explained by coupling of the responses from red‐sensitive and green‐sensitive elements each of which has properties otherwise similar to single red‐sensitive and green‐sensitive cones.
The electrical response of turtle cones to flashes and steps of light
Authors: Baylor D. A. , Hodgkin A. L. , Lamb T. D. 
Published: December 2014

1. The linear response of turtle cones to weak flashes or steps of light was usually well fitted by equations based on a chain of six or seven reactions with time constants varying over about a 6‐fold range.2. The temperature coefficient (Q10) of the reciprocal of the time to peak of the response to a flash was 1·8 (15‐25° C), corresponding to an activation energy of 10 kcal/mole.3. Electrical measurements with one internal electrode and a balancing circuit gave the following results on red‐sensitive cones of high resistance: resistance across cell surface in dark 50–170 MΩ; time constant in dark 4‐6·5 msec. The effect of a bright light was to increase the resistance and time constant by 10–30%.4. If the cell time constant, resting potential and maximum hyperpolarization are known, the fraction of ionic channels blocked by light at any instant can be calculated from the hyperpolarization and its rate of change. At times less than 50 msec the shape of this relation is consistent with the idea that the concentration of a blocking molecule which varies linearly with light intensity is in equilibrium with the fraction of ionic channels blocked.5. The rising phase of the response to flashes and steps of light covering a 105‐fold range of intensities is well fitted by a theory in which the essential assumptions are that (i) light starts a linear chain of reactions leading to the production of a substance which blocks ionic channels in the outer segment, (ii) an equilibrium between the blocking molecules and unblocked channels is established rapidly, and (iii) the electrical properties of the cell can be represented by a simple circuit with a time constant in the dark of about 6 msec.6. Deviations from the simple theory which occur after 50 msec are attributed partly to a time‐dependent desensitization mechanism and partly to a change in saturation potential resulting from a voltage‐dependent change in conductance.7. The existence of several components in the relaxation of the potential to its resting level can be explained by supposing that the ‘substance’ which blocks light sensitive ionic channels is inactivated in a series of steps.
The inhibitory effect of the cerebellar fastigial stimulation on ADH secretion
Authors: Hata Namiyo , Miura Mitsuhiko 
Published: December 2014

1. Both cardiovascular and antidiuretic hormone (ADH) responses to some neural inputs were examined in paralysed anaesthetized cats.2. Carotid occlusion elicited cardiovascular responses and increased ADH secretion. When the electrical stimulation of discrete loci of the cerebellar fastigial nucleus (fastigial pressor area) was superimposed on carotid occlusion, cardiovascular responses were further facilitated, while ADH secretion was inhibited.3. The fastigial stimulation alone elicited facilitory cardiovascular responses composed of hypertension and tachycardia, and the fastigial pressor response (FPR), but did not evoke any consistent ADH response.4. These facts indicate that cerebellar modulation of ADH secretion occurs not directly via the hypothalamo‐hypophysial system but through the lower brain stem to which both carotid sinus nerves and outflows from the fastigial pressor area project.5. We conclude that the fastigial pressor area is specific for not only cardiovascular and other autonomic responses but pituitary hormonal response.
Responses of olfactory bulb neurones to odour stimulation of small nasal areas in the salamander
Authors: Kauer John S. , Moulton David G. 
Published: December 2014

1. Previous experiments have suggested that one way odours may be discriminated is by different spatial patterns of response at both the olfactory bulb and receptor level. The present experiments were designed to test to what extent the position of an odour on the receptor mucosa can influence the activity of olfactory bulb neurones.2. To deliver odours to small areas on the nasal receptor sheet a new method for local application of odour was developed. The flow rate, concentration, and time course of the odour were controlled using the olfactometer described in the preceding paper.3. In thirty olfactory bulb units in the salamander it was found that if the response of a unit to odour delivered to the entire exposed receptor epithelium were suppression (type S), then the unit tended to be suppressed when odour was delivered to a number of localized epithelial regions. If the response were excitation (type E) to stimulation of the entire epithelium, then stimulation to only one or two localized regions would elicit the maximum response.4. Different epithelial regions had the ability to cause excitation in the same bulbar unit depending on the odour being used. Two odours, camphor and amyl acetate, elicited maximum excitation when they were presented to different mucosal areas. The areas at which presentation of these odours gave excitation were surprisingly consistent from unit to unit and animal to animal.5. The data presented here suggest the presence of restricted excitatory receptive fields for some olfactory bulb neurones for a particular odour.6. The presence of spatial response patterns using odour delivery to small nasal receptor regions and thus the presence of receptive fields is discussed with reference to bulbar neuronal circuitry.
Axonal surface charges: binding or screening by divalent cations governed by external pH
Authors: D'arrigo J. S. 
Published: December 2014

1. The effect of different extracellular alkaline‐earth cations (Ca2+, Mg2+, Sr2+, Ba2+) upon the threshold membrane potential for spike initiation in crayfish axon has been studied by means of intracellular micro‐electrodes. This was done at the following pHs of the bathing saline: 6·00, 5·35, 5·00, and 4·65 ± 0·05.2. At pH 6·00, the four alkaline earths had essentially the same effect upon the threshold membrane potential.3. At pH 5·35 or lower, it was found that equal concentrations of the alkaline‐earth cations did not have the same effect on the threshold potential. The selectivity sequences observed at the different pHs were: pH 5·35, Ca2+ > Mg2+ > Sr2+ ≥ Ba2+; pH 5·00, Ca2+ ≃ Ba2+ > Sr2+ ≥ Mg2+; pH 4·65, Ba2+, Sr2+ > Ca2+ > Mg2+.4. It is shown that the individual selectivity sequences are predicted rather closely by the equilibrium selectivity theory for alkaline‐earth cations.5. It is concluded that the only difference between excitable cells which show screening and those which bind divalent cations is the net density of ionized, surface acidic groups in the region of the sodium gates.
A mechanism for spike frequency adaptation
Authors: Partridge L. D. , Stevens C. F. 
Published: December 2014

1. Spike frequency adaptation was studied in large neurones of the marine molluscs Archidoris montereyensis and Anisodoris nobilis. These cells respond to a current step with a rapid rise in spike frequency followed by a gradual decline to a new steady level.2. An exponentially declining current, Is, was measured when the cell was voltage clamped following an adapting spike train. The initial amplitude of this current depended on the preceding number of spikes and on the voltage to which the cell was clamped. A reversal potential (Vs) for this current was obtained by clamping to various potentials following a spike train. The time constant (τs) of decay of the current was dependent upon the clamping potential.3. Clamping the membrane potential to a constant test level from various initial levels initiates an exponentially decaying current of similar time constant. The voltage dependence of the steady‐state conductance (ḡsas(V, ∞)) associated with this current was determined using this technique.4. Equations for neural repetitive firing (Connor & Stevens, 1971c) were modified by the addition of a term describing these slow membrane currents: [Formula: see text]. The solution to the modified equation was in good agreement with the spike frequency adaptation observed in these cells.