bluuebunny/crossref_metadata_2025 huggingface dataset:
Barium‐treated mammalian skeletal muscle: similarities to hypokalaemic periodic paralysis.
Authors: Gallant E M
Published: December 2014

In vivo, Ba2+ produces flaccid paralysis of mammalian skeletal muscle and lowers serum K+ concentration. An episode of hypokalaemic periodic paralysis (h.p.p.) produces similar changes. Reduced K+ permeability may be involved in the onset of h.p.p., and Ba2+ is known to block K+ channels in some types of excitable cells. I have investigated the mechanism of Ba2+ action in mammalian skeletal muscle (mouse and pig) in vitro. Ba2+ (1‐10 mM) initially potentiated twitch force but subsequently depressed both twitches and tetani. These effects were enhanced by low external K+ concentration (0 mM) and diminished by doubling the external K+ (8 mM). Muscle paralysed by Ba2+ responded to caffeine (25 mM) or K+ (100‐200 mM) with a contracture. The Ca2+ channel blocker verapamil did not prevent paralysis and, in fact, enhanced Ba2+ depression of tetani. Mouse long digital extensor (e.d.l.) muscles were depolarized by approximately 35 mV after 5 min in the presence of 1 mM‐Ba2+. Action potentials from porcine muscles exposed to Ba2+ for 30 min rose and fell more slowly than controls and thus had a longer duration. Continuous recordings of membrane potential from individual cells revealed that 5 mM‐Ba2+ depolarized mouse e.d.l. muscle at about 0.05 times the rate with high K+ (200 mM). I conclude that Ba2+ acts relatively slowly to block K+ channels, to decrease K+ fluxes and to induce depolarization. The rate of spontaneous inactivation of the contraction was apparently faster than the rate of activation. This would account for the Ba2+‐induced flaccid paralysis without an initial contracture. These results with Ba2+‐treated muscle illustrate similarities to h.p.p. and indicate that Ba2+ may create a useful model for studies relevant to h.p.p. Furthermore, Ba2+ may provide an appropriate means for evaluating K+ channel function in other muscle disorders.
Alpha and beta‐adrenergic mediation of membrane potential changes and metabolism in rat brown adipose tissue.
Authors: Girardier L , Schneider‐Picard G
Published: December 2014

Membrane potential and flavoprotein redox state have been measured simultaneously and continuously in brown adipose tissue in order to determine how nerve stimulation and adrenergic agonists control its metabolic activity. Both trains of nerve impulses and addition of noradrenaline evoke two temporally distinct cell depolarizations. The first rapid depolarization precedes the increase in flavoprotein reduction. With nerve stimulation, at the time of maximum flavoprotein reduction the cell has repolarized or hyperpolarized. The second slow depolarization follows flavoprotein reduction. Phentolamine, an alpha antagonist, selectively blocks the first depolarization, but not the flavoprotein reduction. However the time of maximum flavoprotein reduction is delayed. Propranolol, a beta antagonist, delays the first repolarization until the end of nerve stimulation and inhibits the transient hyperpolarization, second depolarization and flavoprotein reduction. Isoproterenol, a beta agonist, or the fatty acid octanoate produce only a transient hyperpolarization and subsequent slow depolarization following flavoprotein reduction. Thus brown adipose tissue contains both alpha‐ and beta‐adrenergic receptors. Stimulation of alpha receptors produces an early membrane depolarization. Stimulation of beta receptors leads to an increase in metabolic activity which then appears to produce slow changes in membrane potential.
Perception of colour in unilateral tritanopia.
Authors: Alpern M , Kitahara K , Krantz D H
Published: December 2014

The unilateral tritanope described in the previous paper (Alpern, Kitahara & Krantz, 1983) was able to match every narrow‐band light presented to his tritanopic eye with lights from a tristimulus colorimeter viewed in the adjacent field by the normal eye. In two regions of the spectrum (called isochromes) physically identical lights appeared identical to the observer's two eyes. One isochrome was close to ‘blue’ for the normal eye, the other was in the long‐wave spectral region seen by the normal eye predominantly as ‘red'. Between these isochromes the normal eye required less than spectral purity to match, dropping to near zero purity at 560‐570 nm. A mixture of the two isochromes that appeared purple to the normal eye appeared neutral to the tritanopic eye. Hence dichoptic matches grossly violate Grassmann's additivity law. For the normal eye colour naming conformed to typical normal results. For the tritanopic eye the results were coherent with those found by dichoptic matching: the spectrum was divided into two regions by the achromatic neutral band. To the short‐wave side, only the colour names ‘blue’ and ‘white’ were ever used. To the long‐wave side the predominant colour names were ‘red’ and ‘white’ with some ‘yellow'. Spectral lights appeared neither ‘red‐blue’ nor greenish. Surrounding the test with an annulus either 430 nm, 650 nm, or a mixture of these, fails to induce any greenish appearance, although the achromatic band shifted in the expected directions. It is concluded that there must be exactly three functionally independent, essentially non‐linear central codes for colour perception, and that these codes are different from those suggested in existing theories of colour perception.
The control of tonic tension by membrane potential and intracellular sodium activity in the sheep cardiac Purkinje fibre.
Authors: Eisner D A , Lederer W J , Vaughan‐Jones R D
Published: December 2014

Intracellular Na activity (aiNa) was measured with recessed‐tip, Na‐selective micro‐electrodes in voltage‐clamped sheep cardiac Purkinje fibres. Tension was measured simultaneously. aiNa was increased reversibly either by exposing the preparation to K‐free, Rb‐free solution of by adding the cardioactive steroid strophanthidin. An increase of aiNa produced an increase of tonic tension which was larger at depolarized membrane potentials. At sufficiently negative membrane potentials, changes of aiNa (over the range 6‐30 mM) had no effect on tonic tension. Therefore, both an increase of aiNa and a depolarization are required to increase tonic tension. It is concluded that either a low level of aiNa or a large negative membrane potential is sufficient to maintain a low intracellular Ca concentration. Tonic tension was measured as a function of aiNa. At a given membrane potential the relationship can be described empirically by an equation of the form: tonic tension = b(aiNa)y, where y is a constant and b depends on membrane potential. In five experiments y was found to be 3.7 +/‐ 0.7 (mean +/‐ S.E.M.) over a range of potentials from ‐60 to ‐10 mV. Tonic tension was measured as a function of membrane potential. At a given aiNa the relationship can be described approximately as: tonic tension = k exp (aV), where a is a constant and k depends on aiNa. In five experiments a was found to be 0.06 +/‐ 0.01 mV‐1 (mean +/‐ S.E.M.). A depolarization of 10 mV increases tonic tension by the same amount as does an increase of aiNa that is equivalent to a 3.7 mV change of the Na equilibrium potential, ENa. Hence ENa is nearly 3 times more effective than membrane potential in controlling tonic tension. During a prolonged depolarization (several minutes) the initial increase of tonic tension decays gradually. This is associated with a fall of aiNa. The relationship between tonic tension and aiNa is similar to that seen when aiNa is increased by inhibiting the Na pump. It is concluded that the fall of aiNa is responsible for the decay of tonic tension. The changes of tonic tension reported in this paper are consistent with the effects of aiNa and membrane potential on a voltage‐dependent Na‐Ca exchange. The possibility that a voltage‐dependent Ca channel contributes to tonic tension is also discussed.
Effects of combined carotid chemoreceptor and atrial receptor stimulation on renal blood flow in anaesthetized dogs.
Authors: Kappagoda C T , Karim F , Mackay D
Published: December 2014

In dogs anaesthetized with chloralose and artificially ventilated, carotid chemoreceptors were stimulated by changing the perfusate of the vascularly isolated carotid bifurcations from arterial to venous blood. Left atrial receptors were stimulated by distending balloons in two pulmonary vein‐left atrial junctions and in this left atrial appendage. The left renal blood flow was measured by an electromagnetic flow meter at a constant systemic (renal) arterial pressure in preparations in which heart rate changes were prevented by administration of propranolol hydrochloride (0.5 mg kg‐1) and atropine sulphate (0.4 mg kg‐1). Muscular movement was prevented by gallamine triethiodide (0.2 mg kg‐1). Stimulation of left atrial receptors resulted in a significant increase (P less than 0.001) in renal blood flow of 5.6 +/‐ 0.88 ml min‐1 100 g‐1 renal mass from a control of 223 ml min‐1 100 g‐1 renal mass. The responses were abolished by cooling the cervical vagus nerves to 6‐8 degrees C. Stimulation of carotid chemoreceptors, by perfusion of the carotid bifurcations by venous blood, caused a decrease in renal blood flow of 20 +/‐ 6.9 ml min‐1 100 g‐1 renal mass from 224 ml min‐1 100 g‐1 renal mass. Stimulation of left atrial receptors during venous perfusion of carotid chemoreceptors resulted in an increase in renal blood flow of 10.9 +/‐ 1.82 ml min‐1 100 g‐1 renal mass from 208 ml min‐1 100 g‐1 renal mass. These results show that atrial receptors and chemoreceptors can interact in their effects on renal blood flow.
The effect of cellular energy reserves and internal calcium ions on the potassium conductance in skeletal muscle of the frog.
Authors: Fink R , Hase S , Lüttgau H C , Wettwer E
Published: December 2014

The increase in K+ conductance induced by repetitive stimulation in metabolically poisoned sartorius muscle fibres of the frog was investigated, using a two‐micro‐electrode voltage‐clamp technique. After the inhibition of creatine kinase by 0.4 mM‐1‐fluoro‐2,4‐dinitrobenzene (FDNB) and a complete and irreversible exhaustion of contractility, a nearly linear current‐voltage relation was measured between ‐100 and 0 mV. In the presence of CN‐ (4 mM) an ‘intermediate state’ could be established by repetitive stimulation towards complete mechanical exhaustion. In this labile state, the high and potential‐independent K+ conductance could be induced by repetitive voltage‐clamp pulses (100 ms duration) from ‐85 to 0 mV membrane potential. After the pulses had ceased, fibres regained their original membrane conductance within several minutes. After the electrophoretic injection of the Ca2+‐chelating agent H2EGTA2‐ into fibres in the intermediate state, an increase in membrane conductance by repetitive voltage‐clamp pulses could no longer be induced. Fibres in the intermediate state into which H2EGTA2‐ ‐buffered Ca2+ (free Ca2+ approximately 10(‐5) M) was injected, or to which external caffeine (1.5 mM) was applied, showed a spontaneous and reversible increase in membrane conductance. In metabolically poisoned and mechanically exhausted sartorius muscles the concentrations of creatine phosphate (CP) and ATP were estimated using biochemical standard methods. The concentration of CP remained basically unchanged after FDNB poisoning. In solutions containing CN‐ plus iodoacetate CP fell below the detectable concentration of about 0.5‐1% of the normal value. ATP decreased to slightly less than 20% under both conditions. It is concluded that internal free Ca2+ promotes the activation of the K+ conductance in exhausted muscle fibres, and that a shortage of energy reserves increases the ‘sensitivity’ of K+ channels to Ca2+ ions.
The 4‐6 HZ tremor during sustained contraction in normal human subjects.
Authors: Gottlieb S , Lippold O C
Published: December 2014

Continuous elevation of the middle finger for 15‐60 min gave rise to modulation of the e.m.g. at 4‐6 Hz. A marked peak (50‐150% of the amplitude of the coexisting 8‐12 Hz peak) at 4‐6 Hz was produced in sixteen out of twenty‐one subjects. The 8‐12 Hz peak was also enhanced (2‐14 times with respect to its initial amplitude in eighteen subjects) during the course of the prolonged contraction but its frequency did not change. The 4‐6 Hz and the 8‐12 Hz peaks were present simultaneously; it is concluded that the two phenomena are separate entities. A step‐function mechanical perturbation of the finger generates, time‐locked to the stimulus, a train of waves at the frequency of the slow tremor, which can be abolished by local ischaemia. It is proposed that this slow tremor is due to an oscillatory process, possibly involving the reflex arc, but entailing a longer neuronal delay than that responsible for 8‐12 Hz tremor.
Conduction velocities of corticospinal axons in the rat studied by recording cortical antidromic responses.
Authors: Mediratta N K , Nicoll J A
Published: December 2014

The rat corticospinal tract was stimulated at the medullary pyramid and at different levels in the spinal cord (segments C2/3, T2, T12) and responses were recorded from the surface of the cerebral cortex and extracellularly from individual cortical neurones. Irrespective of the site stimulated, the earliest surface and single unit responses had frequency‐following and other characteristics which indicated they resulted from antidromic invasion of corticospinal neurones. Synaptically mediated discharges with longer latency were also evoked in cortical neurones other than corticospinal neurones. At least in part these discharges probably resulted from stimulus spread to the dorsal column‐medial lemniscus pathway. Corticospinal neurones were almost all between 1.0 and 1.5 mm beneath the cortical surface while synaptically excited units were at all depths greater than 0.4 mm. By stimulating at two sites, estimates of conduction velocity were obtained for single corticospinal axons. For those reaching at least as far as T12, velocities caudal to the pyramid ranged from 5 to 19 m/s (mean 11.4 +/‐ 2.9 m/s; S.D.). Slow axons in the pyramid (antidromic latency greater than 2.5 ms) could rarely be excited from T12. By stimulating at three sites (pyramid, T2, T12) most axons reaching T12 were found to have similar conduction velocities in the ‘cervical’ (pyramid‐T2) and ‘thoracic’ (T2‐T12) cord. However, in 15% of the axons the ‘thoracic’ velocity was at least 25% less than the cervical. The results are discussed and related to those from previous investigations.
Effect of stimulation or lesioning of the hypothalamus upon gonadotrophin secretion in the guinea‐pig.
Authors: Donovan B T , Gnanathankom M G
Published: December 2014

The effect of electrical stimulation of the anterior hypothalamus of the guinea‐pig upon follicle‐stimulating hormone (FSH) and luteinizing hormone (LH) secretion during two phases of the oestrous cycle was examined and compared with the response to electrolytic or radio‐frequency lesions placed in the same area. The secretion of LH was briefly increased by electrical stimulation of the hypothalamus, with a greater response occurring over days 7‐8 (luteal phase) of the oestrous cycle than on days 13‐14 (follicular phase). An equivalent rise in LH output was produced by placement of direct current (d.c.) lesions in the hypothalamus, whereas lesions made with radio‐frequency current produced a small increase only on days 13‐14. The secretion of FSH was not changed by any procedure.
Strength‐duration characteristics of myelinated and non‐myelinated bulbospinal axons in the cat spinal cord.
Authors: West D C , Wolstencroft J H
Published: December 2014

Strength‐duration characteristics for the stimulation of 131 raphespinal and reticulospinal axons in the spinal cord were determined using two types of stimulating electrode. Conduction velocity of these fibres ranged from 0.86 to 63 m/s. With silver wire (250 micron diameter) stimulating electrodes, chronaxies were: 0.18 +/‐ 0.06 ms for axons conducting between 16 and 63 m/s, 0.4 +/‐ 0.22 ms for axons conducting between 5 and 15 m/s and 2.06 +/‐ 0.79 ms for those with conduction velocity less than 5 m/s. There was an inverse relationship between chronaxie and conduction velocity. Rheobase values ranged from 7.4 to 400 microA but were independent of conduction velocity. Chronaxies obtained with wire electrodes were compared with those from stimulation of the same fibre through saline‐filled micropipettes (2‐12 micron tip diameter). Rheobase values with the micropipettes ranged from 1.6 to 20 microA, indicating a close proximity of the pipette to the axon. For these axons, chronaxies from metal wire electrodes ranged from 0.12 to 2.4 ms and for micropipettes from 0.04 to 0.65 ms. In almost all cases, chronaxies for micropipette stimulation were lower than those for metal wire electrodes. Furthermore, with micropipettes chronaxies were independent of conduction velocity. The results are shown to be related to differences in time constant of the activated region of axon and charge requirements of threshold activation. The two stimulating conditions, i.e. micro‐electrodes compared with wire electrodes, are analogous to the theoretical point stimulated cable and uniformly polarized membrane cases. The results are discussed in relation to the possibility of determination of fibre type from stimulation characteristics. A distinction between chronaxies of myelinated and non‐myelinated fibres can be made using wire electrodes of 250 micron diameter, but not with micro‐stimulation, as with micropipettes (2‐12 micron diameter).
Somatic and visceral inputs to the thoracic spinal cord of the cat: effects of noxious stimulation of the biliary system
Authors: Cervero F.
Published: December 2014

1. Single unit electrical activity has been recorded extracellularly from 133 neurones in the grey matter of the 8th and 9th thoracic segments of the spinal cord in chloralose anaesthetized cats. The responses of these neurones to electrical stimulation of the ipsilateral splanchnic nerve, to natural stimulation of the skin and to distension of the biliary system have been studied.

2. Of the neurones studied, 75% responded to electrical stimulation of the splanchnic nerve and had a cutaneous receptive field in the costal region (viscero‐somatic neurones). Twenty‐three per cent of the neurones had a cutaneous receptive field but no visceral input (somatic neurones) and 2% had a visceral input but no cutaneous field.

3. Somatic neurones had well‐localized receptive fields from which they could be driven by innocuous stimulation of the skin (52%), by noxious (7%) or by both forms of stimulation (41%). No somatic neurones projected to supraspinal levels via the contralateral ventro‐lateral funiculus.

4. Viscero‐somatic neurones were excited by small myelinated and non‐myelinated afferent fibres in the splanchnic nerve. Most viscero‐somatic neurones had cutaneous inputs from nociceptors either exclusively (38%) or in addition to non‐noxious inputs (53%).

5. The recording sites of somatic neurones were located almost exclusively in laminae II and IV and dorsal V of the dorsal horn. In contrast, viscero‐somatic neurones were located in lamina I and in laminae V—IX of the grey matter. No differential distribution of recording sites according to type of cutaneous receptive field has been found within the viscero‐somatic group of neurones.

6. About one‐third of all viscero‐somatic neurones could be excited by distensions of the biliary system. In all cases, intensities of visceral stimulation above physiological levels were necessary to activate the neurones. Most units driven by biliary afferents were located in or ventral to lamina V of the dorsal horn. The excitation of these units by biliary distension was found to be specifically mediated by receptors in the biliary system.

7. Sixteen per cent of the neurones were found to project to supraspinal levels via crossed ventro‐lateral pathways. All of these neurones were viscero‐somatic with axonal conduction velocities between 12 and 68 m sec−1.

8. These results are discussed in relation to the postulates of the ‘Convergence‐projection’ theory of referred pain.
Effects of exposure to lines of one or two orientations on different cell types in striate cortex of cat.
Authors: Hirsch H V , Leventhal A G , McCall M A , Tieman D G
Published: December 2014

We raised cats using goggles to control early visual exposure (stripe‐rearing). Four conditions were used: (a), both eyes exposed to 0 degrees lines, (b), both eyes exposed to 90 degree lines, (c), one eye exposed to 45 degree lines, the other to 135 degree lines, (d), one eye exposed to 0 degree lines, the other to 90 degree lines. At the completion of the rearing, we recorded extracellularly from single cells in striate cortex (area 17) of these animals; circular statistics were used to analyse the distribution of the orientation preferences of neurones recorded. Exposure to either one or two stimulus orientations produced a significant bias in the distribution of the orientation preferences of cells recorded. We found no more non‐selective cells in cats exposed to one orientation (15%) than in cats exposed to two orientations (14%). We found about the same mean proportion of binocular cells in cats exposed to one orientation (27%) as in cats exposed to two orientations (24%). Cells were comparable in orientation selectivity in cats exposed to one orientation (mean half‐width at half‐height = 37 degrees) and in cats exposed to two orientations (mean half‐width at half‐height = 34 degrees). The effects of the rearing depended upon the receptive field properties of the cells. For cells with narrow receptive fields and low cut‐off velocities, the rearing produced no bias in the distribution of the orientation preferences; for all other groups of cells the rearing produced a bias toward the exposed orientation. In addition, the cells with narrow receptive fields and low cut‐off velocities were more finely tuned for orientation than the remaining cells. We conclude that there are cell types in the striate cortex of the cat which differ in their susceptibility to the effects of stripe‐rearing; these cell types can be discriminated on the basis of their physiological characteristics. We can compare these cell types with morphologically identified cell types that also differ in their susceptibility to the effects of stripe‐rearing.
Simultaneous visualization of aortic and [3H]5‐hydroxytryptamine‐accumulating cell bodies in the nodose ganglion of the cat
Authors: Gaudin-Chazal G. , Portalier P. , Puizillout J. J. , Vigier D.
Published: December 2014

1. Single‐ and double‐tracer experiments were performed in cats to investigate the relationship between the aortic cells and the cell bodies accumulating 5‐hydroxytryptamine (5‐HT) in the nodose ganglion. In one series of experiments, horseradish peroxidase (HRP) was applied to the central end of the aortic nerve, anterogradely transported and accumulated in ganglionar perikarya. The distribution of HRP‐positive neurones was reconstructed in serial sections through the nodose ganglion. In a second series of experiments, the distribution of [3H]5‐HT‐accumulating cell bodies was assessed following incubation of the nodose ganglion in [3H]5‐HT. The third series of experiments combined the treatments of the preceding ones: anterograde transport of HRP in the aortic nerve followed by incubation of the nodose ganglion in [3H]5‐HT.

2. The results from these experiments provide more information with regard to (i) the topographical relationship between the aortic and [3H]5‐HT‐accumulating cell bodies in the same ganglion and (ii) the distribution and number of double‐labelled neurones, giving further indications about histochemical components of the aortic nerve.

3. The HRP experiments demonstrated that HRP‐positive cells show a preferential pattern of topographical organization. They were mostly located in the medial border of the ganglion where the laryngeal and aortic nerves enter. On the other hand, [3H]5‐HT‐accumulating neurones were scattered throughout the ganglion.

4. In double‐tracer experiments, three populations of labelled cell bodies were distinguished in the same nodose ganglion: (1) single HRP‐cells; (2) single [3H]5‐HT‐accumulating cells and (3) double‐labelled cells. The distribution of the latter population exhibited no preferential localization. Quantitative estimates indicated that double‐labelled neurones constituted 65‐85% of the population of HRP‐positive cell bodies.

5. These results show that most aortic neurones are able to take up exogenous serotonin and may be serotonergic neurones. They suggest that serotonin may be involved in physiological effects mediated via the aortic nerves.
Possible functions of the interhemispheric connexions between visual cortical areas in the cat.
Authors: Blakemore C , Diao Y C , Pu M L , Wang Y K , Xiao Y M
Published: December 2014

The functions of interhemispheric axons linking the borders between cortical areas 17 and 18 on the two sides of the brain were investigated by two techniques. A well‐matched sample of neurones was recorded in the 17/18 border region before and after an extensive lesion was made in the corresponding part of the other hemisphere. The proportion of binocularly driven cells fell from 96% to 67%, confirming the results of Dreher & Cottee (1975). Orientation‐and direction‐selectivity, as well as the responsiveness of the population of neurones, seemed unaltered. The reduction in binocularity was much less convincing for cells in the body of area 17, even very close to the callosal‐recipient zone. Reversible cooling of the 17/18 border had no effect on the few cells recorded outside the callosal zone in the other hemisphere nor on eighteen of the thirty‐five cells recorded in the callosal zone. However, in ten cells the receptive field disappeared completely in one eye; in five cells there was a general reduction in responsiveness; two cells lost a portion of the receptive field, on the ipsilateral side, in both eyes. The receptive fields that were apparently transmitted via the corpus callosum lay around the vertical meridian of the visual field and were not restricted to the visual hemifield ipsilateral to the receiving hemisphere: their distribution overlapped that provided by the direct geniculo‐cortical input. The principal function of the callosal projection between the 17/18 borders may be to contribute to binocular convergence on cortical cells and perhaps to play a part in stereoscopic vision.
The relationship between soleus and gastrocnemius muscle activity in conscious cats‐‐a model for motor unit recruitment?
Authors: Hodgson J A
Published: December 2014

Force and electromyogram (e.m.g.) data were recorded from medial gastrocnemius and soleus muscles of conscious cats using chronically implanted devices. A digital computer was used to take simultaneous samples of the data from both muscles and construct two‐dimensional frequency distributions relating the activities in the two muscles. The results show that posture is the only activity where soleus may be active without corresponding activity in the medial gastrocnemius muscle. In locomotion the ratio between soleus and medial gastrocnemius muscle activities changed with treadmill speed, although peak soleus force remained constant at approximately 80% of the isometric tetanic tension measured in terminal experiments. A hypothesis is put forward, associating these findings with the activities of slow and fast motor units and emphasizing the influence of neural activity in the determination of motor unit recruitment.
Shared reflex pathways of group I afferents of different cat hind‐limb muscles.
Authors: Harrison P J , Jankowska E , Johannisson T
Published: December 2014

The convergence of group I muscle afferents of different muscle origin onto interneurones in spinal reflex pathways has been investigated using the technique of spatial facilitation of the transmission from afferents to motoneurones. The investigated pathways are those of non‐reciprocal inhibition and of oligosynaptic excitation of motoneurones. Extensive convergence has been found of group I afferents from muscles operating at the same and different joints onto the interneurones interposed in both excitatory and inhibitory, disynaptic and trisynaptic pathways to motoneurones. Convergence has been found between muscle spindle Ia and/or tendon organ Ib afferents from different muscles, thereby extending observations on convergence of these subgroups of group I afferents from the same muscles. The results show that group I afferents of different muscles influence motoneurones via shared neuronal pathways and that transmission from these afferents is influenced by afferents originating in other muscles. The afferent information forwarded to individual motoneurones is therefore the ensemble picture of the length and tension of many muscles.
Electrical and mechanical activity recorded from rabbit urinary bladder in response to nerve stimulation.
Authors: Creed K E , Ishikawa S , Ito Y
Published: December 2014

Responses of the smooth muscle membrane of the rabbit bladder to intramuscular nerve stimulation were investigated by the micro‐electrode and double sucrose‐gap methods. The cell generated regular spontaneous action potentials. Acetylcholine produced a maintained increase in the frequency and ATP a transient increase. Noradrenaline only increased the frequency at very high concentrations. Application of short current pulses (50 microseconds) produced an initial excitatory junction potential (e.j.p.) with a superimposed spike, followed by a late depolarization. On some occasions, hyperpolarization of the membrane appeared between initial e.j.p. and the late depolarization. All these responses were abolished by tetrodotoxin. The late depolarization was enhanced by pre‐treatment with neostigmine and abolished by atropine. This means that the delayed depolarization is due to activation of the muscarinic receptor. When the late depolarization was abolished, the amplitude of hyperpolarization was enhanced. The e.j.p. and contraction were unaffected by guanethidine, phentolamine, methysergide, mepyramine, quinidine or theophylline. This means that the e.j.p. is not mediated by activation of adrenergic, tryptaminergic, histaminergic or purinergic receptors. ATP reduced the amplitude of the e.j.p. due to depolarization of the membrane and reduction in the membrane resistance. The amplitude of the e.j.p. was gradually reduced by repetitive stimulation (0.5‐2.0 Hz). However, the rate of depression was unchanged in the presence of ATP. Dipyridamole did not change the electrical and mechanical responses to field stimulation. These results do not support the proposal that ATP is the non‐cholinergic excitatory transmitter. Apamine and tetraethylammonium (TEA) suppressed the hyperpolarization produced by field stimulation but guanethidine did not inhibit the hyperpolarization. Therefore, the hyperpolarization is due to increased K conductance of the membrane but it is not possible to conclude whether this component is due to the inhibitory action of a neurotransmitter or solely to after hyperpolarization of the spike. It was concluded that the rabbit bladder receives both cholinergic and noncholinergic excitatory neurones.
Low‐frequency characteristics of intracellularly recorded receptor potentials in guinea‐pig cochlear hair cells.
Authors: Russell I J , Sellick P M
Published: December 2014

Intracellular receptor potentials were recorded from inner and outer hair cells in response to low‐frequency tones, from the basal, high‐frequency region of the guinea‐pig cochlea. The receptor potentials recorded from inner hair cells are asymmetrical about the resting membrane potential with the depolarizing phase, which corresponds to rarefaction in sound pressure, exceeding the phase of hyperpolarization by a factor of about 3. It was found that the relationship between the peak‐to‐peak voltage responses and sound pressure level could be described by rectangular hyperbolae. When the frequency of the sound stimulus was progressively increased from 100 Hz to 4 kHz, the ‘periodic’ (a.c.) component of the receptor potential was attenuated with respect to the ‘continuous’ (d.c.) component. The characteristics of the inner hair cells could be described by two stages of low‐pass filtering, with one of the filters having the same corner frequency as the electrical time constants which varied in different cells between 178 and 840 Hz. Receptor potentials recorded intracellularly from two morphologically identified outer hair cells were symmetrical about the resting membrane potential (about ‐65‐70 mV) and had a maximal amplitude of only 5 mV at frequencies and intensities which yield 20‐30 mV voltage responses from inner hair cells. No d.c. component receptor potentials were recorded in response to high‐frequency tones. Phase and amplitude measurements were made from receptor potentials from inner hair cells, and from ‘cochlear microphonic potentials’ which were recorded from the organ of Corti and scala tympani. The phase of depolarization in both potentials was associated with displacement of the basilar membrane towards the scala vestibuli. The phase of the intracellular receptor potentials leads the cochlear microphonic by about 90 degrees and the sound pressure by about 180 degrees at frequencies below 100 Hz. Above this frequency the phase lead progressively declines and at higher frequencies becomes a phase lag. These phase relationships indicate that inner hair cells respond to the velocity of the basilar membrane at frequencies below 200‐600 Hz, and to its displacement above this, and that the voltage responses of the inner hair cells are limited by their membrane time constants. It is suggested that outer hair cells respond to basilar membrane displacement throughout their frequency range. It is shown that, with respect to frequency, the different growth rates of the cochlear microphonic potentials and inner hair cell receptor potentials, and the dominance of cochlear microphonic potentials in the organ of Corti, result in an effective electrical interaction between inner hair cells and cochlear microphonic potentials.
Influence of vasopressin and calcium on electrolyte transport across isolated colonic mucosa of the rat.
Authors: Bridges R J , Nell G , Rummel W
Published: December 2014

Vasopressin enhanced the absorption of water and Na+ across everted sacs of rat colon descendens but had no effect on absorption across the colon ascendens. The short‐circuit current (Isc) and open‐circuit potential difference (p.d.) across the colon descendens were dose‐dependently decreased by vasopressin. Isc and p.d. across the colon ascendens were not altered by vasopressin. In the colon descendens the decrease in Isc and p.d. was significant at 1 microu. vasopressin/ml and reached a maximum at 1 mu./ml. Propranolol and phentolamine or naloxone did not alter the decrease in Isc and p.d. to a submaximal dose of vasopressin. Vasopressin increased the mucosal to serosal flux of Na+ and Cl‐ and decreased the serosal to mucosal flux of Cl‐ across short‐circuited colon descendens. Consequently these changes increased the net flux of Na+ and Cl‐. Adenylate cyclase activity in homogenates of the colon descendens was not altered by vasopressin. Omission of Ca2+ from the serosal bathing solution reversibly decreased Isc and p.d. and increased Na+ and Cl‐ absorption across the colon descendens in a similar way as did vasopressin. The results suggest that the effect of vasopressin on the colon descendens may be due to a decrease in intracellular Ca2+ activity.
The basis for the membrane potential of quiescent cells of the canine coronary sinus.
Authors: Boyden P A , Cranefield P F , Gadsby D C , Wit A L
Published: December 2014

During prolonged periods of quiescence, the membrane potential of cells in the isolated canine coronary sinus, exposed to normal Tyrode solution containing 4 mM‐K, declines to about ‐60 mV. The nature of the resting potential was investigated, in small strips of coronary sinus tissue mounted in a fast‐flow system, by recording the membrane potential responses to sudden changes in the extracellular ionic environment. At extracellular K concentrations ([K]o) from 0 to 64 mM the resting potential was little affected by replacing all but 1 mM of external Cl ions with isethionate and methylsulphate ions. At [K]o levels from 4 to 150 mM the resting potential was reasonably well described by the Goldman‐Hodgkin‐Katz equation on the assumption that the intracellular K concentration ([K]i) was 155 mM and that the ratio of membrane permeability coefficients for Na and K, PNa/PK, was 0.07. In the presence of a high concentration of acetylcholine or carbachol (greater than or equal to 1 microM), the resting potentials at [K]o levels from 1 to 150 mM approximated K equilibrium potentials (EK) calculated on the assumption that [K]i was 155 mM. At [K]o levels less than or equal to 8 mM replacing most of the external Na with sucrose or Tris caused a substantial hyperpolarization, whereas application of 1‐2 microM‐tetrodotoxin caused only slight hyperpolarization. A transient hyperpolarization, due to enhanced electrogenic Na extrusion, was recorded on switching back to 4 mM‐K following brief exposures to K‐free solution; no transient hyperpolarization was recorded in the presence of 5 microM‐acetylstrophanthidin. The acetylstrophanthidin itself caused a rapid depolarization of several millivolts. Preliminary conductance measurements made with two micro‐electrodes in some smaller preparations indicate that the steady‐state current‐voltage relationship is N‐shaped. We conclude that the low membrane potential of quiescent coronary sinus cells reflects not a low [K]i but rather a relatively high ratio PNa/PK, of about 0.07: the Na ions flow into the cells via predominantly TTX‐insensitive pathways and are extruded by the electrogenic Na/K exchange pump, which thereby makes a substantial contribution to the resting potential.
Noradrenaline hyperpolarizes cells of the canine coronary sinus by increasing their permeability to potassium ions.
Authors: Boyden P A , Cranefield P F , Gadsby D C
Published: December 2014

The mechanism of the noradrenaline‐induced hyperpolarization was investigated in small strips of coronary sinus tissue mounted in a fast‐flow system. The recorded hyperpolarization was negligibly small in response to 10 nM‐noradrenaline but was maximal at 10 microM (average amplitude 23 mV, in 4 mM‐K solution). The hyperpolarization was unaffected by 1 microM‐phentolamine but was abolished by 10 microM‐propranolol and so is presumably mediated via beta‐adrenoceptors. The noradrenaline‐induced hyperpolarization became smaller when the extracellular K concentration ([K]o) was raised or when the extracellular Na concentration was lowered. These results are consistent with two general mechanisms: noradrenaline might cause hyperpolarization by stimulating the Na/K pump to generate more outward current, as previously suggested for other cell types. Alternatively, noradrenaline might lower the permeability ratio, PNa/PK, by reducing the permeability coefficient for Na (PNa) and/or increasing that for K (PK). The noradrenaline‐induced hyperpolarization is not diminished during exposure to 5 microM‐acetylstrophanthidin, or to K‐free solution, or to K‐free solution containing acetylstrophanthidin. We conclude that the hyperpolarization does not reflect enhanced electrogenic pump activity. Conductance measurements using two micro‐electrodes in very small preparations revealed that, like the muscarinic agonist carbachol, noradrenaline caused an increase in membrane slope conductance. Steady‐state current‐voltage curves obtained in the presence of noradrenaline, in the presence of carbachol, and in the absence of both drugs all crossed each other at about the same level of membrane potential. During the maintained injection of sufficiently large hyperpolarizing current, application of either noradrenaline or carbachol causes depolarization instead of hyperpolarization. The cross‐over or ‘reversal’ potentials of current‐voltage curves, determined with and without the drugs, vary with [K]o approximately as does the K equilibrium potential calculated assuming the intracellular K concentration to be 155 mM. We conclude that, like carbachol and acetylcholine, noradrenaline causes a specific increase in the K permeability of coronary sinus cells.
Correlation of growth hormone secretion to sleep in the immature rat.
Authors: Kawakami M , Kimura F , Tsai C W
Published: December 2014

The correlation between growth hormone (GH) secretion and the sleep‐wakefulness cycle in the 29‐31 day‐old male rat was studied by serial blood sampling through an intracardiac cannula at 10 min intervals from 12.00 to 18.00 h. E.e.g.s recorded continuously during the blood sampling period were scored into wakefulness and sleep, and the amount of sleep for every 10 min was plotted against the GH value as assessed by radioimmunoassay. The power spectrum analysis and the least‐squares method applied to the time series of GH concentrations in the control rat, revealed that the mean periodicity was 3.12 +/‐ 0.09 h (mean +/‐ S.E. of the mean) in fourteen rats examined. For the animals in which the e.e.g. was recorded simultaneously with blood samplings, the cross‐correlation analysis performed between the time series of the amount of sleep and the GH value revealed a significant positive correlation between the GH level and the amount of sleep during the preceding 10 min. The time series of the sleep amount and the GH value had mean periodicities of 3.09 +/‐ 0.17 and 3.05 +/‐ 0.13 h (mean +/‐ S.E. of the mean), respectively, in twenty‐seven rats examined. 5. Sleep deprivation performed between 13.00 and 15.00 h was effective in preventing GH secretory bursts which otherwise should appear during this time period of the day. 6. Corticosterone measurement by protein‐binding assay revealed that the procedure of sleep deprivation did not act as the ‘stress’ which has been known to inhibit GH secretion in the rat. These findings indicate that GH secretion in the rat is sleep‐related, as has been proved in the human.
Effect of hypoxia on polysynaptic hind‐limb reflexes of unanaesthetized fetal and new‐born lambs.
Authors: Blanco C E , Dawes G S , Walker D W
Published: December 2014

Polysynaptic reflex excitation of the hind‐limb flexor muscles was produced by stimulation of the distal peroneal or common sciatic nerve in ten fetal and six new‐born unanaesthetized lambs. In the fetal lambs, stimulation at 1.1‐3.25 times threshold for direct activation of the nerve produced a reflex response which was greatest during high‐voltage electrocortical activity, being reduced 69 +/‐ 5.0% (mean +/‐ S.E. of the mean) during low‐voltage electrocortical activity. Reduction of the fetal arterial PO2 from 23.3 +/‐ 0.58 to 12.2 +/‐ 0.4 mmHg caused a rapid and reversible reduction of the reflex in all fetal lambs with intact spinal cord, including two whose brain stems were transected at the level of the colliculi. Hypoxia did not alter the amplitude of the reflex in two fetuses in which the spinal cord at L1‐2 had been cut several days previously. In new‐born lambs reduction of the arterial PO2 to 43 mmHg did not change the reflex amplitude during episodes of quiet wakefulness or slow‐wave sleep. Brief reduction of the Pa,O2 to 20‐30 mmHg caused a statistically insignificant reduction of reflex amplitude during quiet sleep before behavioural arousal. It is concluded that hypoxaemia activates reticular mechanisms in the pons and medulla of fetal lambs which decrease the excitability of spinal reflex pathways. In the new‐born lamb such effects are counteracted or prevented by mechanisms associated with arousal.
The influence of deformation of transformed erythrocytes during flow on the rate of oxygen release.
Authors: Kon K , Maeda N , Shiga T
Published: December 2014

The deoxygenation rates of transformed erythrocytes were compared with those of normal discocytes by both stopped‐flow and continuous‐flow methods. Echinocytic and spherostomatocytic transformations were induced by various anionic and cationic drugs, respectively, without altering the oxygen affinity of haemoglobin, the cell volume or the membrane fluidity. The echinocytic transformation reduced the deoxygenation rate at slow‐flow velocities (50 cm/sec), as detected by the continuous‐flow method. However, at higher flow velocities (150 cm/sec) the rate was similar to that seen in normal discocytes. A close correlation between the degree of echinocytosis, the retardation of deoxygenation rate and the increase of suspension viscosity were observed. Microscopic observation of flowing erythrocytes revealed that the echinocytes scarcely deformed at the slower flow velocity, but clearly deformed at the higher flow velocity to various shapes resembling the flowing discocytes. Transformation to spherostomatocytes had no effect on the deoxygenation rate, which was comparable with that of the discocytes, and even the higher flow force did not induce any deformation. The retarded deoxygenation and the increased viscosity of echinocytes was probably due to an augmented stagnant layer around the cells (i.e. an increase of the hydrodynamic effective volume); this layer was reduced when the echinocytes were deformed with increasing flow force.
Effect of aprotinin on the renal response to vasopressin in diabetes insipidus rats.
Authors: Fejes‐Toth G , Frölich J C , Naray‐Fejes‐Toth A
Published: December 2014

The renal response to arginine vasopressin was investigated with and without the simultaneous administration of the kallikrein inhibitor, aprotinin, in conscious Brattleboro homozygous rats with hereditary diabetes insipidus. Arginine vasopressin caused a marked antidiuretic response (urinary osmolality increased from 118 to 739 mosmol/l) which was accompanied by a significant increase in urinary prostaglandin excretion (prostaglandin E2 and F2 alpha excretion increased by 182 and 441%, respectively). Kallikrein excretion remained unchanged after arginine vasopressin infusion. The infusion of aprotinin diminished urinary kallikrein activity to undetectable levels, decreased potassium excretion significantly and caused a slight fall in urinary prostaglandin excretion. However, aprotinin failed to modify the arginine vasopressin‐induced enhancement in prostaglandin excretion (prostaglandin E2 and F2 alpha excretion increased by 168 and 442%, respectively), and the antidiuretic response was also similar to that observed under control conditions. These results indicate that the kallikrein‐kinin system is not involved in the renal response to vasopressin in the Brattleboro rat.
Inhibition of human red cell sodium and potassium transport by divalent cations.
Authors: Ellory J C , Flatman P W , Stewart G W
Published: December 2014

The influx and efflux of Na and K across the human red cell membrane by the bumetanide‐sensitive (Na‐K co‐transport) and residual (ouabain‐ and bumetanide‐insensitive) routes were inhibited by increasing concentrations of external Mg. Ca, Sr, Ba, Mn and Co also inhibited bumetanide‐sensitive and residual K transport. External Mg inhibited choline uptake and the Na‐dependent fractions of L‐alanine and L‐serine uptakes. External Mg reduced the maximal rate (app. Vmax) but not the affinity (app. Km) of the bumetanide‐sensitive K and Na influxes when they were measured as functions of external K and Na respectively. The inhibitory effect of Mg was not due to a small reduction in zeta potential since much larger reductions in zeta potential produced by neuraminidase did not affect transport. Internal Mg stimulated the ouabain‐sensitive K influx but inhibited the co‐transport and residual components of K influx. Bumetanide was a poor co‐transport inhibitor in red cells pre‐treated with A23187 and EDTA. It was concluded that the inhibitory effects of external Mg were probably not due to changes in the ionic composition of the diffuse double layer adjacent to the cell membrane. Mg and other divalent cations should not be used as ‘inert’ ionic substitutes in human red cell Na and K transport studies.