bluuebunny/crossref_metadata_2025 huggingface dataset:
Renin dependence of captopril‐induced drinking after ureteric ligation in the rat.
Authors: Elfont R M , Fitzsimons J T
Published: December 2014

In experiments lasting 8 h, low (0.5 mg kg‐1) or medium (5 mg kg‐1) subcutaneous doses of the angiotensin‐converting enzyme inhibitor captopril were mildly dipsogenic in sham‐operated rats, much more so in rats subjected to bilateral ureteric ligation and not at all in bilaterally nephrectomized rats. Rats with ligated ureters drank enough water to gain weight during the experiments. All other groups lost weight. The enhanced responsiveness of rats with ligated ureters, despite fluid retention, shows that captopril‐induced drinking was not secondary to increased renal fluid loss. Ureteric ligation alone which caused some increase in renin secretion was mildly dipsogenic compared with sham operation. Captopril caused further increases in plasma renin concentration and more drinking suggesting that the captopril response is renin‐dependent. The failure of the nephrectomized rat to drink after captopril also shows that the response is renin‐dependent. The highest dose (50 mg kg‐1) of captopril did not at first stimulate drinking, though water intake increased later. Slowness to drink was not the result of general depression of behaviour since drinking in response to subcutaneous hypertonic NaCl or intracranial angiotensin II was not inhibited by the highest dose. Slowness to drink after the highest dose was attributable to blockade of converting enzyme centrally as well as peripherally. This meant that the increased circulating angiotensin I resulting from peripheral blockade of converting enzyme was only slowly converted to angiotensin II in the brain. When cerebral conversion of angiotensin I was prevented by a single intracranial injection of 25 micrograms captopril, drinking in response to the lower doses of captopril was also inhibited in normal rats and in rats with ligated ureters. The same intracranial dose of captopril also inhibited drinking in response to intracranial injections of renin or angiotensin I, but not angiotensin II. The time course of inhibition of renin‐induced drinking was similar to that of inhibition of subcutaneous captopril‐induced drinking. In conclusion, subcutaneous captopril causes increased water intake through activation of the renal renin‐angiotensin system, an effect that is enhanced when the system has already been partly activated by ureteric ligation. Increased circulating angiotensin I resulting from blockade of peripheral converting enzyme must be converted to angiotensin II in the brain in order to stimulate drinking. Drinking is not the consequence of increased fluid loss.
Role of cross‐bridge distortion in the small‐signal mechanical dynamics of insect and rabbit striated muscle.
Authors: Thorson J , White D C
Published: December 2014

The mechanism of the active tension response of insect fibrillar muscle to step changes and small oscillations of length was re‐investigated, following White's demonstration (1983) that the high relaxed stiffness evidently persists during activation and cannot be neglected as had previously been assumed. White's result makes earlier explanations of the small‐signal response untenable; the experimental and theoretical studies described here lead to a new class of explanations at the cross‐bridge level. The response of an activated muscle to a fast stretch consists of a synchronous tension increase that is followed first by a rapid decay of tension and then by a delayed rise ('stretch activation'). It was shown in glycerinated fibre preparations from the water bug and the bumblebee that subtraction of the relaxed tension response from the active response results in a prominent undershoot of the tension level preceding the step, before the delayed rise of tension. The responses of the same fibres to sinusoidal oscillations, in the frequency range 1‐150 Hz, showed an equivalent behaviour, with the active locus circling the relaxed locus in a Nyquist plot, as described by Machin & Pringle (1960). Stiffness was determined during the tension response to a large step (of 1%) by recording the immediate change of tension to a small test step (0.2%), applied at various times after the conditioning step. In the majority of preparations stiffness remained constant or increased during the undershoot of tension. Step and sinusoidal responses with the above features cannot be explained at all by an active component resembling a simple exponential delay. We show, however, that such features are predicted if certain small‐signal effects of cross‐bridge distortion (previously and erroneously assumed negligible in insect flight muscle for the small‐signal case) are incorporated in models of the cross‐bridge cycle. Two alternative hypotheses for the effects of distortion are examined: (i) distortion‐induced detachments and (ii) distortion‐modulated transitions among multiple attached states (Huxley & Simmons, 1971). For the first we also show that the results do not differ qualitatively whether one assumes strain, interfilament displacement or ‘bridge recruitment’ as the physical correlate of stretch activation. Both of the above explanations account, at least qualitatively, for the observed rapid decay and undershoot of tension following a step increase of length, and for the circling of the active Nyquist‐plot loci about the passive locus. The explanation based on distortion‐induced detachments, however, appears to be inconsistent with the stiffness measurements.(ABSTRACT TRUNCATED AT 400 WORDS)
The time course of synaptic potentials evoked in cat spinal motoneurones at identified group Ia synapses.
Authors: Redman S , Walmsley B
Published: December 2014

Excitatory post‐synaptic potentials (e.p.s.p.s) were evoked in motoneurones by impulses in single group Ia axons. After recording the e.p.s.p., the motoneurone and the group Ia axon were injected with horseradish peroxidase. The morphological details of the connexion formed by each group Ia axon with a motoneurone were subsequently reconstructed. Four Ia axon‐motoneurone pairs were obtained. The electrotonic distance from the soma to each synaptic bouton in the connexion was calculated. The electrotonic lengths of those dendrites on which synaptic connexions were found were also calculated. The shape indices of each recorded e.p.s.p. and the standard cable model of the motoneurone were used to calculate the electrotonic distance from the soma to the point on the equivalent dendritic cable at which the e.p.s.p. originated. This distance was compared with the distance obtained from the reconstruction of the synaptic connexion at which the e.p.s.p. was generated. For two of the four connexions, the locations calculated by both methods agreed to within 0.1 lambda. Similar agreement could only be obtained for the other two connexions if synaptic transmission did not occur at some of the boutons in the termination. Evidence that some boutons were not involved in transmission is presented in the following paper (Redman & Walmsley, 1983).
The effect of catecholamines on intestinal glucose and oxygen uptake in the dog.
Authors: Grayson J , Oyebola D D
Published: December 2014

Using the anaesthetized dog, continuous recording was made of the oxygen and glucose contents of the artery and the vein draining the upper jejunum. Flow was also measured and results expressed as differences in oxygen and glucose between the aorta and the jejunal vein (a‐v), also as oxygen consumption and glucose uptake. Resting glucose uptake was greater than could be accounted for on the basis of oxidation. When adrenaline (1 microgram/kg. min) or noradrenaline (2 micrograms/kg. min) was infused intravenously, oxygen uptake rose by about 50% whereas glucose uptake rose by 300‐500%; moreover, the rise in glucose uptake was apparent before the rise in oxygen uptake. The beta‐blocking agent, propranolol (0 X 5 mg/kg. min) had no effect on oxygen uptake but caused a three‐fold rise in glucose uptake. Subsequently infusion of adrenaline had no effect on oxygen uptake and no effect on glucose uptake. However, on stopping the infusion there was a marked drop in glucose uptake, which was not maintained. It is suggested that the effects of catecholamines may be due to altered arterial blood glucose levels and that the jejunum may play a role in glucose homeostasis which requires the action of beta receptors.
Inhibitory interactions between interneurones in reflex pathways from group Ia and group Ib afferents in the cat.
Authors: Brink E , Jankowska E , McCrea D A , Skoog B
Published: December 2014

A hypothesis has been verified that laminae V‐VI interneurones which mediate non‐reciprocal inhibition of motoneurones from group I muscle afferents have collateral actions on other laminae V‐VI interneurones. Stimulation within the areas of projection of these inhibitory interneurones in motor nuclei and in Clarke's column would be expected to give rise to monosynaptic i.p.s.p.s in interneurones with disynaptic i.p.s.p.s from group I afferents if the hypothesis were correct. Intracellular records were made from eighty‐five laminae V‐VI interneurones with input from group Ia muscle spindle and/or group Ib tendon organ afferents. Weak intraspinal stimuli applied in motor nuclei in L7 and S1 segments, or in the lateral funiculus just caudal to Clarke's column in L4, were found to evoke monosynaptic i.p.s.p.s in seventy‐two interneurones. These i.p.s.p.s were systematically correlated with disynaptic inhibition from group Ia or Ib afferents but not from other fibres. Such monosynaptic i.p.s.p.s evoked by intraspinal stimuli were seen in forty‐two interneurones which themselves projected to the level of Clarke's column and therefore (on the basis of previous evidence) should mediate inhibition of motoneurones. For seven of these interneurones it was also shown directly that they projected to motor nuclei. The inhibition of such interneurones demonstrates mutual interactions between those interneurones which are interposed in inhibitory pathways from group I afferents. Only indirect indications have been obtained for inhibition of interneurones in the excitatory pathways.
The effect of intracellular calcium on the sodium pump of human red cells.
Authors: Brown A M , Lew V L
Published: December 2014

The inhibitory effect of cytoplasmic Ca on Na‐pump‐mediated Na‐K exchange was investigated in intact red cells under conditions of constant cell volume, membrane potential and inorganic ion composition. The ionized cytoplasmic Ca concentration ( [Ca2+]i) was controlled using the ionophore A23187. In normal cells, ouabain‐sensitive 24Na efflux was inhibited with an apparent affinity for [Ca2+]i which depended on the concentration of A23187; 50% inhibition required 20‐40 microM and 160‐300 microM‐cytoplasmic Ca2+ with 10 microM and 0.63 microM‐A23187 respectively. Cytoplasmic Ca also affected cell ATP content which fell rapidly on addition of A23187 and subsequently increased, steadied or continued to fall more slowly depending on the Ca and A23187 concentrations. Half‐maximal fall required 5‐15 microM and 110‐170 microM‐cytoplasmic Ca2+ at 10 microM and 0.63 microM‐A23187 respectively. Removal of Ca from the cells failed to reverse either the Na pump inhibition or the fall in cell ATP. In ATP‐enriched cells cytoplasmic Ca caused inhibition of ouabain‐sensitive 24Na efflux in an A23187‐dependent manner with apparent affinities for [Ca2+]i similar to those observed in the normal cells. Inhibition was complete at high [Ca2+]i. As in the normal cells, the ATP content of the cells fell in the presence of cytoplasmic Ca, but always remained above 1.2 m‐mole/l. cells. This was higher than the ATP content of Ca‐free normal intact cells. A23187 had no effect on the inhibition by Ca of ouabain‐sensitive ATPase activity in isolated red cell membrane preparations. Both under conditions near optimal for Na‐K‐ATPase activity and under conditions resembling those in the cytoplasm, inhibition was half‐maximal at about 25 microM‐Ca2+ and in the latter case complete at below 400 microM‐Ca2+. The apparent ATP‐dependence of ouabain‐sensitive Na efflux in the presence of cytoplasmic Ca was distinctly different in the normal and ATP‐enriched cells but in both groups of cells it was similar for data obtained with high and low concentrations of A23187. The data for Na pump inhibition by cytoplasmic Ca in the intact cells were well fitted by several kinetic models involving either [Ca2+]i or CaATP as the inhibitory species and a low affinity dependence of pump activity on MgATP or total ATP. However, for any model, the apparent affinities for CaATP or for Ca2+ required to fit the ATPase data were 2.5‐10 times higher than those required to fit the data for Na efflux.(ABSTRACT TRUNCATED AT 400 WORDS)
The effect of increased lung volume on the expiratory rate of rise of alveolar carbon dioxide tension in normal man.
Authors: Edwards A D , Jennings S J , Newstead C G , Wolff C B
Published: December 2014

The rate at which alveolar PCO2 (PA, CO2) rises during expiration has been measured in seven healthy medical students. PA, CO2 rate of rise [delta PA, CO2/delta t] was measured by a method utilizing constant expiratory flow rates in individual breaths in two subjects, and was calculated from airway PCO2 and expiratory tidal volume in the remaining five subjects. Steady‐state runs were recorded at two or more metabolic rates with the subject making no special effort to control mean lung volume. This was done to establish the relationship between delta PA, CO2/delta t and the rate of CO2 production (VCO2) at normal lung volume in individual subjects. Steady‐state runs were also recorded at high lung volume. In each subject delta PA, CO2/delta t was less than would have been obtained at normal lung volume. Inversion of a hypothetical relation between delta PA, CO2/delta t, VCO2 and average lung volume (VLa; DuBois, Britt & Fenn, 1952) yielded calculated values of VLa for both the normal and the high lung volume states. Lung gas volume was measured in a whole body plethysmograph, ('box volume') both for the normal and high lung volume states, in each subject. Mean VLa and ‘box volume’ estimates showed only moderately good agreement, whereas the estimated differences between normal and high lung volume obtained by the two methods were virtually identical. These experiments suggest that the expiratory PA, CO2 rate of rise is determined, in the steady state, partly by the rate of CO2 production (a directly proportional relationship) and partly by the mean lung volume (an inversely proportional relationship).
Maintenance of cholinergic neurones and synapses in the ciliary ganglion of aged rats.
Authors: Wigston D J
Published: December 2014

The ciliary ganglion has been examined in young adult (1.5‐2 months) and aged rats (24‐28 months). In young adult rats the ganglion contains about 200 neurones, each of which is innervated by 1‐4 preganglionic axons (mean, 2.2). In these animals about 2‐3 X 10(3) synaptic boutons were observed per square millimetre in thin sections of the ganglion; synapses were located mainly on finger‐like extensions of cell bodies and on dendrites. The size of the ganglion cell population, the number of inputs per ganglion cell, the density of synaptic boutons and the amplitude of post‐synaptic potentials recorded intracellularly did not differ significantly between the young and aged animals. It thus appears that the neuronal population of the ciliary ganglion and the cholinergic synapses received by ganglion cells are remarkably stable well into old age.
Changes in threshold for calcium transients in frog skeletal muscle fibres owing to calcium depletion in the T‐tubules.
Authors: Miledi R , Parker I , Zhu P H
Published: December 2014

Strength‐duration curves were measured for voltage‐clamp depolarizations required to elicit a just detectable rise in intracellular calcium, as monitored using arsenazo III, in frog twitch muscle fibres. In normal Ringer solution, the threshold for a 5 sec duration depolarization was about 5 mV more negative than for a 200 msec duration pulse. The shift in threshold comparing 200 msec and 5 sec pulses was almost abolished in bathing solutions including magnesium or nickel (4 mM), or where the free calcium concentration was buffered. The shift in threshold was little changed by substitution of barium for calcium. These results can be explained by supposing that the 5 sec depolarization activates an inward calcium flux across the T‐tubule membrane, which decreases the calcium concentration in the tubules, and hence alters the threshold for activation of excitation‐contraction (e.‐c.) coupling because of surface charge effects.
The variation in shortening heat with sarcomere length in frog muscle.
Authors: Homsher E , Irving M , Lebacq J
Published: December 2014

Pairs of frog semitendinosus muscles were stimulated tetanically for 2 s at 0 degree C and, after 0.75 s of isometric contraction, were released at constant velocity for 0.16 s. The distance shortened was 0.3 micron per sarcomere. The extra heat (shortening heat) associated with the release was determined by comparison with isometric control tetani. The mean sarcomere length at the start of stimulation was varied between 2.25 and 3.75 microns. At the greater initial lengths there was considerable resting tension and heat was absorbed during releases of unstimulated muscles. This thermoelastic effect was also present during stimulation, so shortening heat values were calculated from the difference between the heat production of the stimulated and unstimulated muscle for releases over the same length range and at the same velocity. Laser diffraction was used to measure mean sarcomere length in the part of the muscle from which heat was recorded. At the greater initial lengths these central sarcomeres slowly elongated by a small amount during nominally isometric tetani. When a release was given during a tetanus the central sarcomere shortening was slightly less than that in a release of the unstimulated muscle with the same change of muscle length. In the period of a tetanus after the release had ended the rate of central sarcomere elongation was greater than that in an isometric tetanus. Shortening heat production had a large early component, during and just after the release, then continued to increase slowly up to the end of the tetanus. It is likely that sarcomere length redistribution along the muscle is responsible for the apparent slow phase, but has little effect on the early component. Shortening heat (determined as the early component) decreased linearly with increasing muscle length in the range studied. The intercept on the length axis was 3.78 +/‐ 0.08 micron per sarcomere (mean +/‐ S.E. of mean, n = 7, based on sarcomere length before stimulation). The corresponding intercept for the isometric tension before the release was 3.78 +/‐ 0.03 micron per sarcomere. The isometric heat rate at this time also decreased with increasing muscle length, but at 3.75 microns per sarcomere was still 50.0 +/‐ 2.0% of its maximum value. The results suggest that shortening heat, like isometric tension, is produced by the interaction of thick and thin filaments in contracting muscle.
The intracellular pH of frog skeletal muscle: its regulation in hypertonic solutions.
Authors: Abercrombie R F , Roos A
Published: December 2014

Intracellular pH (pHi) was followed with micro‐electrodes in frog semitendinosus muscle, superfused at 22 degrees C with hypertonic solutions (external pH, pHo, 7.35) containing 2.5, 15 or 50 mM‐K. Tonicity was doubled by addition of 250 mM‐mannitol or, in a few cases, 125 mM‐extra NaCl. Tripling of tonicity was accomplished by adding 500 mM‐mannitol. Because of the ability of hypertonicity to minimize contracture, the course of pHi could be followed from the start of depolarization. The pHi of fibres after about 40 min in Ringer solution (2.5 mM‐K, HEPES buffer) of twice normal tonicity was 7.40 +/‐ 0.04 (S.E. of mean) (n = 17), about 0.2 higher than at normal tonicity. The membrane potential, Vm, was ‐87.7 +/‐ 1.3 mV. When the muscle was depolarized in 50 mM‐K to about ‐30 mV, the pHi rapidly fell by 0.3‐0.5 unit (n = 9), and then promptly returned. This recovery was followed by a much slower and progressive rise to above control. Removing Na from the medium did not affect the degree of acidification, but the pHi recovered at a slightly slower rate, did not reach control value and showed no progressive rise. A less pronounced transient acidification was also observed when the muscle was depolarized in 15 mM‐K to about ‐60 mV. When contracture was prevented either by 1‐2 mM‐tetracaine under isotonic conditions or by raising tonicity 3‐fold, 50 mM‐K produced no transient acidification. When the pHi of resting fibres in Ringer solution (2.5 mM‐K) of twice normal tonicity was reduced by 5% CO2 from 7.40 to 7.12 +/‐ 0.07 (n = 3), it recovered at a slow rate (0.06 +/‐ 0.03 delta pHi h‐1). Depolarization by 15 or 50 mM‐K enhanced recovery rate 4‐6‐fold. These solutions of twice normal tonicity, as compared to those of normal tonicity, shifted the curve relating pHi recovery rate and membrane potential along the potential axis in the direction of hyperpolarization. This shift may be due to increased ionic shielding of fixed negative charges at the inner membrane surface. At twice normal tonicity, the very slow pHi recovery of resting fibres from CO2‐induced acidification, as well as the more rapid recovery in depolarized fibres, could be abolished by 1 mM‐amiloride or by removing Na. The application of amiloride during pHi recovery in 50 mM‐K was not associated with an observable change in Vm. SITS had no significant effect on recovery.(ABSTRACT TRUNCATED AT 400 WORDS)
Transmitter release during normal and altered growth of identified muscle fibres in the crayfish.
Authors: Lnenicka G A , Mellon D
Published: December 2014

During growth of identified crayfish muscle fibres from a diameter of 20 to 400 micron, the excitatory junctional potential (e.j.p.) amplitude was found to be independent of diameter. Thus, e.j.p. amplitude was maintained during growth in spite of a 21‐fold decrease in miniature excitatory junctional potential (m.e.j.p.) amplitude previously reported (Lnenicka & Mellon, 1983). The maintenance of e.j.p. amplitude was found to be partially due to a 5‐fold increase in quantal release at ‘active sites’ during growth. In order to determine whether the increase in transmitter release can be regulated by the rate of muscle fibre growth, the rate of growth was experimentally reduced. By decreasing the resting length of the muscle during growth, the rate of increase in the diameter was reduced by approximately 50% compared with the contralateral control muscle fibres. The input resistance and the m.e.j.p. were appropriately larger in the smaller‐diameter experimental fibres. However, e.j.p. amplitude in the experimental fibres was not significantly different from that in the contralateral control fibres. This was apparently due to the significantly smaller quantal release at active sites on the experimental fibres compared with control fibres. Thus, experimental alteration of the rate of muscle fibre growth results in regulation of transmitter release, suggesting that the muscle fibre may control the increase in transmitter release seen during normal growth.
Segmental actions of afferents of the interosseous nerve in the cat.
Authors: Harrison P J , Johannisson T
Published: December 2014

Electrical stimulation of the interosseous nerve evokes oligosynaptic inhibition of extensor motoneurones and excitation of flexor motoneurones. Lowest‐threshold, shortest‐latency post‐synaptic potentials evoked at group I strength are attributed to the action of group Ib afferents. Post‐synaptic potentials evoked at slightly higher stimulus strengths (within the higher group I and the group II range) and at longer latency are attributed to the action of afferents of Pacinian corpuscles. Facilitation of post‐synaptic potentials evoked from afferents in the interosseous nerve by group I muscle afferents and by joint afferents is taken to indicate convergence of these afferents onto common interneurones in reflex pathways to motoneurones. Evidence is presented that afferents of Pacinian corpuscles project to the interneurones mediating group I (non‐reciprocal) reflex actions to motoneurones. Unitary monosynaptic excitatory post‐synaptic potentials (e.p.s.p.s) evoked from the interosseous nerve are taken to indicate that only a very small number of muscle spindle Ia afferents course through the interosseous nerve. Dorsal root potentials evoked by low‐strength electrical stimulation of the interosseous nerve are largely attributable to the action of afferents of Pacinian corpuscles.
Roles of extrajunctional receptors in the response of guinea‐pig mesenteric and rat tail arteries to adrenergic nerves.
Authors: Itoh T , Kitamura K , Kuriyama H
Published: December 2014

Studies of the electrical response of isolated guinea‐pig mesenteric and rat tail arteries to perivascular nerve stimulation were made by micro‐electrodes inserted from the outer surface of the vessels. Membrane potential of both arteries was ‐68 to ‐69 mV and usually stable, though with occasional miniature excitatory junction potentials (m.e.j.p.s). Perivascular nerve stimulation produced excitatory junction potentials (e.j.p.s) which usually increased in size with repetitive stimulation, particularly in the mesenteric artery, but rarely triggered a spike or other regenerative response. Phentolamine and yohimbine in low concentrations increased the size of the e.j.p.s in both arteries, and increased the mechanical response of the mesenteric artery, probably by blocking prejunctional alpha 2 receptors which depress release of noradrenaline by the nerves; they reduced the mechanical response of the tail artery, probably by blocking alpha 2 receptors of the smooth muscle. Prazosin in low concentration had no effect on the e.j.p.s but inhibited contraction in both arteries, probably by blocking alpha 1 receptors of the smooth muscle. In the tail artery, but not the mesenteric artery, e.j.p.s produced by repetitive perivascular nerve stimulation were followed by a slow depolarization reaching a maximum at about 20 s and then decaying over 1‐3 min; it did not reach the threshold for contraction, assessed by K depolarization. Yohimbine reduced the size and duration of the slow depolarization. High concentrations of noradrenaline (10(‐5) M) caused depolarization and contraction of the mesenteric artery, both of which were blocked by prazosin and little affected by yohimbine. In the tail artery, yohimbine did but prazosin did not block the depolarization produced by any concentration of noradrenaline, although yohimbine was almost as effective as prazosin in blocking the contraction produced by low concentrations of noradrenaline. Extrajunctional adrenoceptors in the mesenteric artery therefore included high sensitivity types of alpha 1 receptor, and in the tail artery high sensitivity types of alpha 1 and alpha 2 receptor. Some of the extrajunctional receptors, as well as the junctional receptors responsible for e.j.p.s in both arteries, produced depolarization. Most of the contraction induced by either nerves or exogenous noradrenaline was produced by the extrajunctional receptors, and was not dependent on the depolarization which some of these receptors induced.
Correlation of activity in neighbouring goldfish ganglion cells: relationship between latency and lag.
Authors: Johnsen J A , Levine M W
Published: December 2014

Pairs of retinal ganglion cells in the isolated goldfish retina were recorded simultaneously with a single electrode. Repeated flashes of light were delivered to evaluate the response latency of each of the units. The cross‐correlation histogram for the maintained discharge of each pair of cells was examined, and its temporal relationships (lags) were compared with the differences in response latencies of the two units. There was a strong correlation between these measures; however, the differences between latencies were often at least twice as great as the lags. The differences between the times to the peaks of the responses of the two units were less reliably related to the lags of the pairs, although the correlation was positive and the differences in time‐to‐peak generally greater than the lags. The weaker relationship between the difference in time‐to‐peak and lag than between latency difference and lag is apparently a manifestation of a negative correlation between latency and rise time (from first response to peak). This indicates that cells with a longer latency compensate with a faster rise time. There was a negative correlation between the mean maintained rate of a neurone and its response latency. That is, cells with faster maintained discharge rates respond sooner than those with slower maintained rates. There was virtually no relationship between the lags or the differences in latency and the differences between the magnitudes of the responses to light. Thus, it is unlikely that differences in latency (or lags) could be attributed to unequal effectiveness of the stimuli for the two units. The relationship between differences in latency and lags did not depend on the response categorizations of the two units. Specifically, it did not matter whether the members of the pair were on centre, off centre or on‐off centre; neither did it matter whether they were X‐like or not‐X‐like neurones. Consideration of these data leads to the conclusion that there must be ‘marked’ pathways of differential conduction velocity through the retina.
The central control of fetal breathing and skeletal muscle movements.
Authors: Dawes G S
Published: December 2014

Breathing movements in the sheep fetus have been observed from a gestational age of about 40 days. From 95 to 115 days fetal breathing movements are almost continuous, interrupted by apnoea rarely exceeding 2 min. From 115 days until term (about 147 days) breathing and movements of the trunk and limbs are episodic. Breathing normally occurs only during rapid‐eye‐movement sleep as identified by low‐voltage cortical electrical activity. Active movements of the neck muscles occur predominantly in high‐voltage electrocortical activity. Hypercapnia or acid cerebrospinal fluid perfusion cause an increase in the regularity and depth of breathing when present, and recruit intercostal and laryngeal abductor activity. Isocapnic hypoxia, however, in contrast to the hyperventilation seen postnatally, causes arrest of fetal breathing movements. This effect is due to a central inhibition. Section of the brain stem, from the caudal hypothalamus rostrally, causes dissociation of fetal breathing movements and electrocortical activity into independent rhythms. Section of the brain stem caudally, in the upper pons or at the inferior colliculus, also causes a dissociation of electrocortical activity from breathing movements, which become almost continuous. Isocapnic hypoxia causes an increase in the rate and depth of breathing movements. It is concluded that the arrest of breathing in intact fetal lambs is not due to a direct effect on the respiratory centre in the medulla. The lumbar polysynaptic flexor reflex response becomes episodic after 115 days gestation but, in contrast to fetal breathing movements, is enhanced during high‐voltage electrocortical activity. Isocapnic hypoxia arrests movements of the fetal limbs and trunk and inhibits the lumbar flexor reflex. This inhibition of the reflex is prevented by section of the spinal cord at T12, but persists after section of the brain stem in the upper pons. It is attributed to an action on the medulla, independent of the systemic arterial chemoreceptors. Small doses of pentobarbitone (5 mg/kg) cause arrest of fetal breathing movements by a suprapontine mechanism, abolished by brain stem transection, and inhibition of the lumbar flexor reflex by an action on the spinal cord, persisting after transection at T12. Inhibitors of prostaglandin synthetase (indomethacin, meclofenamate or aspirin) induce continuous fetal breathing movements, while prostaglandin E2 arrests fetal breathing. The site of action is on the medulla, as shown by section of the brain stem and of afferents from the systemic arterial chemoreceptors.(ABSTRACT TRUNCATED AT 400 WORDS)
Central effects of dopamine on vasopressin release in the normally hydrated and water‐loaded rat.
Authors: Forsling M L , Williams H
Published: December 2014

The effect of intracerebroventricular (I.C.V.) micro‐injections of dopamine on vasopressin (AVP) release was investigated in normally hydrated and hydrated rats anaesthetized with urethane, hormone concentrations being determined by radioimmunoassay. Dopamine given in doses of less than 25 micrograms had little effect on AVP concentrations already elevated as a result of anaesthesia and surgery. Doses of over 25 micrograms produced a transient increase in AVP concentrations followed by a fall. Both the increase and the fall were statistically significant. Pimozide (400 micrograms/kg) blocked the fall in AVP concentrations following dopamine. A fall was still seen after the administration of haloperidol (400 micrograms/kg) but it was only significant 20 min after the injection of dopamine. The changes in AVP concentration after the administration of naloxone (400 micrograms/kg) were not statistically significant. In water‐loaded rats I.C.V. micro‐injections of dopamine produced a dose‐dependent antidiuresis over the range 1‐25 micrograms. An injection of 25 micrograms dopamine in these animals produced an increase in AVP concentrations to 1.8 +/‐ 0.51 microunits/ml and a fall in urine flow which could be approximately matched by an infusion of vasopressin of 15 microunits/min. The antidiuresis in response to dopamine could be blocked by haloperidol. The response to dopamine in the anaesthetized animals depends on a number of factors including the initial activity of the neurohypophysial system.
Renal blood flow and its distribution following haemorrhage in the rat: the role of vasopressin.
Authors: Al-Omar Azzawi S , Shirley D G
Published: December 2014

The effect of an acute arterial haemorrhage of 15 ml/kg body weight on renal and intrarenal blood flow (measured using radioactive microspheres) was determined in anaesthetized rats. In order to assess the role of vasopressin in mediating the observed changes, the response to haemorrhage of animals lacking the ability to synthesize vasopressin (Brattleboro rats) was compared with that of the parent strain (Long Evans rats). In addition, a group of Long Evans rats was treated with an antagonist of the vascular action of vasopressin before being bled. Thirty minutes after haemorrhage the mean arterial blood pressure of untreated Long Evans rats was significantly higher than that of Brattleboro or vasopressin antagonist‐treated Long Evans rats. Following haemorrhage, total renal vascular resistance increased markedly in untreated Long Evans rats. In these animals there were substantial increases in calculated vascular resistance in both inner and outer halves of the renal cortex. In Brattleboro rats there was only a small increase in renal vascular resistance, confined to the outer cortex, whilst in vasopressin antagonist‐treated Long Evans rats there was no significant change in the vascular resistance of either cortical region. It is concluded that much of the increase in renal vascular resistance which follows haemorrhage is due to vasopressin. This vasoconstrictor effect of the hormone, which contributes to its pressor action after haemorrhage, occurs in both the inner and outer regions of the renal cortex.
Formation of electrical coupling between embryonic Xenopus muscle cells in culture.
Authors: Chow I , Poo M M
Published: December 2014

Electrical coupling between embryonic Xenopus muscle cells in 1‐5 day old cultures was studied after isolated cells were manipulated into contact for various periods. The coupling was examined by measuring the electrotonic spread of acetylcholine (ACh)‐induced membrane depolarizations or of potential changes induced by intracellular current injection. In 1 day old culture, cells developed coupling rapidly after contact. Strong coupling was observed within 20 min after contact was made. The rate of coupling formation was age dependent. The percentage of cell pairs that established detectable coupling within 30 min of contact decreased from 66% in 1 day culture to 0% in 5 day culture. Older cells, when put into contact for prolonged periods, developed substantial coupling, suggesting that the age of the culture affects the rate of coupling formation rather than the final extent of coupling. Pre‐treatment of older cells with colchicine, metabolic inhibitors, Ca2+ and Mg2+‐free saline, or trypsin significantly increased the rate of coupling formation to a level close to that of younger cells. This suggests that the reduced rate of coupling was not due to a lack of membrane precursors for the intercellular channels, but was probably due to the appearance of extramembranous constraints for the channel assembly.
Studies on the trigeminal antidromic vasodilatation and plasma extravasation in the rat.
Authors: Couture R , Cuello A C
Published: December 2014

Antidromic stimulation of sensory peripheral branches of the trigeminal system (mental nerve) led to cutaneous vasodilatation and increased vascular permeability in rats anaesthetized with urethane. The antidromic vasodilatation observed in intact animals was not altered by decentralization or sympathectomy. Both antidromic vasodilatation and neurogenic plasma extravasation remained unaffected by pre‐treatment with cimetidine, indomethacin, baclofen, guanethidine plus phentolamine and propranolol, but were significantly reduced by cimetidine plus mepyramine and atropine, suggesting that cholinergic and histaminergic components might be involved in the sensory neurogenic responses. Methysergide reduced only the extravasation, suggesting that probably serotonin liberated by mast cells upon sensory stimulation can contribute to the neurogenic responses. In tests using substance P (SP) antagonists (D‐pro4, D‐ trp 7, 9, 10)‐SP (4‐11) and (D‐pro2, D‐trp 7, 9)‐SP it was found that they are more active in reducing the neurogenic extravasation than the vasodilatation. In addition it was observed that (D‐pro 4, D‐trp 7, 9, 10)‐SP (4‐11) was the most potent substance P antagonist in reducing the plasma extravasation and antidromic vasodilatation resulting from sensory stimulation.
Fictive locomotion in the lamprey spinal cord in vitro compared with swimming in the intact and spinal animal.
Authors: Wallén P , Williams T L
Published: December 2014

A comparison has been made of the patterns of muscle activity during swimming in the intact and spinal lamprey, and the patterns of ventral root activity in the in vitro preparation of the lamprey spinal cord. Electromyographic (e.m.g.) activity was recorded with intramuscular bipolar electrodes from three segmental levels in intact lampreys swimming in a swim‐mill at a range of swimming speeds. The patterns of activity obtained were similar to those seen in elasmobranch and teleost fish. After high spinal transection, lampreys could be induced to swim continuously for a period of several minutes in the swim‐mill by a light initial mechanical stimulation of the tail or dorsal fin. The patterns of e.m.g. activity obtained from spinal animals at a range of swimming speeds were similar to those obtained in the intact state. Portions of spinal cord were isolated encompassing those segments from which e.m.g. recordings had been made and ventral root recordings were made in vitro of the rhythmic activity induced by bath application of D‐glutamate. In all experiments the mean duration of the bursts of activity at any segmental level was directly proportional to the mean cycle duration, and the constant of proportionality (about 0.36) was similar for all three types of preparation. In all preparations the mean time delay for the activation of segments in the rostral‐caudal direction was proportional to the cycle duration and to the number of segments between recording positions. The proportionality constant, or phase lag per segment, was approximately equal to 0.01 in all three types of preparation.
Comparison of properties of calcium channels between the differentiated 1‐cell embryo and the egg cell of ascidians.
Authors: Hirano T , Takahashi K
Published: December 2014

In the ascidians Halocynthia roretzi and H. aurantium the Ca channels in the differentiated embryo whose cleavage was arrested with cytochalasin B at the 1‐cell stage and in the unfertilized egg were studied using the voltage‐clamp technique. In the cleavage‐arrested 1‐cell embryo, which differentiates into a cell of epidermal type after culturing until the time of hatching of the control larvae, Ca channel and Ca‐induced K channel currents were observed upon depolarization of the membrane. Inward current through Ca channels in the embryo was analysed after suppressing Ca‐induced K current by intracellular injection of EGTA. Sr or Ba ions could substitute for Ca ions as the charge carrier through Ca channels both in the cleavage‐arrested embryo and in the egg. The selectivity ratios among these cations at their respective maximum inward currents were 1.0 (Ca):2.0 (Sr):4.5 (Ba) for the Ca channel in the embryo and 1.0 (Ca):1.9 (Sr):1.1 (Ba) for that in the egg. The time course of inactivation of Ca channels in Ca artificial sea water (ASW) was different from that in Sr or Ba ASW in the cleavage‐arrested embryo. Fast inactivation was observed only in Ca ASW, and slight and slow inactivation was seen in Ba or Sr solution. In the egg, Ca, Sr and Ba currents through Ca channels all showed a similar time course of inactivation. The time course and voltage dependence of inactivation in Ca ASW were studied by measuring Ca tail current at a constant potential level of ‐28 mV. In the cleavage‐arrested embryo the inactivation became slower and smaller in accordance with the decrease in inward Ca current when the potential level of the command pulse was increased in the positive direction from 10 to 80 mV. In the egg the time course of inactivation became faster when the potential level was similarly increased. The experimental results in (4) and (5) above suggest that the inactivation of the Ca channel in the cleavage‐arrested embryo was dependent on Ca inward current while that in the egg was potential dependent. The developmental changes of Ca channels from egg type to epidermal type were studied in the cleavage‐arrested 1‐cell embryo. The epidermal‐type Ca channels appeared at about 40 h after fertilization at 9 degrees C. The Ca channels in those blastomeres which differentiated to a cell of muscular type in the cleavage‐arrested 8‐ or 16‐cell embryo were studied after suppressing the outward current by tetraethylammonium and by intracellular injection of both Cs ions and EGTA.(ABSTRACT TRUNCATED AT 400 WORDS)
Geometric accommodation between the dimensions of erythrocytes and the calibre of heart and muscle capillaries in the rat.
Authors: Canham P B , Potter R F , Woo D
Published: December 2014

The finer and more closely arrayed the capillaries are, the more efficiently oxygen will be transported to tissue because the same blood volume has greater contact area with the tissue and the diffusion distance for the oxygen is minimized. If these principles are actually governing microvascular structure, then the finest capillaries will be the narrowest channels which circulating erythrocytes can transit. Ascertaining the existence of this geometric limit requires quantitative data of demonstrated reliability on erythrocyte geometry and on capillary diameters. The study was done on Wistar rats. Constant flow perfusion of skeletal and cardiac muscle by a modified Batson's compound for anatomical casting made available rigid three‐dimensional replicas of the microvasculature which shrank less than 1% when the tissue was digested with potassium hydroxide. Measurements of individual capillaries were made on high contrast scanning electron micrographs of the casts. Measurements on individual rat erythrocytes were done on photomicrographs of cells on edge. Reliability of these data was tested in three ways. First, repeatability of the tracing of the cell outline was tested by processing a duplicate set of photomicrographs. Secondly, correlations of the various parameters were found. Thirdly, results from other techniques of measuring erythrocytes were examined for areas of agreement and also for causes of possible error for areas in dispute. Because of known variability in erythrocyte sizes and shapes between species and between individuals within a species, we compared the data on erythrocyte geometry and capillary diameters for samples taken from the same individual rat. The data revealed a very positive indication that the lowest range of capillary diameters were at the limits of deformation of the circulating erythrocytes. Ninety‐five per cent of the erythrocytes sampled could pass through a channel 2.9 micron in diameter. A small number of the capillaries measured were narrower than this limit. The data on erythrocytes and capillaries were compared for six rats. The limiting diameter for passage of erythrocytes was remarkably uniform for all six animals.
Calcium release and sarcoplasmic reticulum membrane potential in frog skeletal muscle fibres.
Authors: Baylor S M , Chandler W K , Marshall M W
Published: December 2014

Single twitch fibres were dissected from frog muscle, stretched to a sarcomere spacing greater than or equal to 3.9 micron, then mounted for optical recording. The experiments were carried out at 15‐17 degrees C. In some cases D2O Ringer solution was used instead of H2O Ringer solution to reduce movement and any related optical artifacts. Following action potential stimulation, both the amplitude and time course of the change in intrinsic retardation (Baylor & Oetliker's second component, 1975) were found to be approximately independent of wavelength between 480 and 750 nm (D2O Ringer solution). Fibres were injected with the Ca2+‐sensitive dye Arsenazo III so that changes in myoplasmic free [Ca2+] could be estimated by measuring changes in dye‐related absorbance at 660 nm. The time course of free [Ca2+] was compared with the time course of two other optical signals which have been previously suggested to monitor s.r. (sarcoplasmic reticulum) membrane potential, intrinsic retardation and Nile Blue A fluorescence (Bezanilla & Horowicz, 1975). In D2O Ringer solution the retardation time course was closely similar to that of free [Ca2+] whereas the fluorescence time course was considerably slower. Thus, it is possible that either the retardation signal or Nile Blue A fluorescence (or both) monitors free [Ca2+] rather than s.r. potential. If so, the underlying mechanism which senses Ca2+ must do so very rapidly in the case of retardation and with a delay in the case of Nile Blue A. Changes in Nile Blue A fluorescence were measured in a voltage‐clamped fibre (H2O Ringer solution). Only small changes were observed during hyperpolarization or small depolarization whereas relatively large changes were observed near mechanical threshold. These increased e‐fold in magnitude every 4‐5 mV. This steep voltage dependence, similar to that already shown for intrinsic retardation and [Ca2+], provides additional evidence that Nile Blue A fluorescence monitors a step in excitation‐contraction coupling. Theoretical waveforms of s.r. membrane potential were computed using a typical waveform of s.r. Ca2+ release (from Baylor, Chandler & Marshall, 1983) under the assumption that Ca2+ crosses the s.r. membrane as electrical current. Voltage waveforms were calculated using several combinations of electrical parameters for the s.r. membrane. Only certain combinations gave theoretical potential changes similar to the intrinsic retardation or Nile Blue A fluorescence signal.(ABSTRACT TRUNCATED AT 400 WORDS)